Enoxaparin as bridging anticoagulant treatment in cardiac surgery.

OBJECTIVE: To assess enoxaparin as bridging anticoagulant treatment in cardiac surgery. METHODS: Prospective registry of those patients who underwent cardiac surgery in our centre between December 2003 and June 2004 and required long-term anticoagulation. Subcutaneous enoxaparin was used as bridging anticoagulant treatment according to a pre-established protocol. The global thromboembolic risk was carefully assessed in all patients. All patients were followed up for 3 months. RESULTS: Of 140 patients who were included (mean (SD) age 66 (11); 49% female), 51 were already receiving long-term acenocumarol treatment before the index intervention. 50% of the patients were at high or very high risk for thromboembolic events in the postoperative period. The mean (SD) number of days between surgery and the first dose of anticoagulant was 2.01 (7) for acenocumarol and 1 (1.01) for enoxaparin. The mean (SD) daily dose of enoxaparin was 1.1 (0.27) mg/kg. Six thromboembolic events (4.3%; 95% CI 1.6 to 9.1) occurred, but only four of them were plausibly related to enoxaparin (2.9%; 95% CI 0.8 to 7.1). Six major haemorrhagic events (4.3%; 95% CI 1.6 to 9.1) occurred, but only three were plausibly related to enoxaparin (2.1%; 95% CI 0.4 to 6.1). CONCLUSIONS: These findings show a reasonable rate of adverse events using enoxaparin as bridging anticoagulant treatment in cardiac surgery. Randomised studies are necessary to evaluate the real efficacy and safety of enoxaparin as bridging anticoagulant treatment in cardiac surgery.

Oral glucose tolerance test is needed for appropriate classification of glucose regulation in patients with coronary artery disease: a report from the Euro Heart Survey on Diabetes and the Heart.

BACKGROUND: Patients with coronary artery disease (CAD) and abnormal glucose regulation (AGR) are at high risk for subsequent cardiovascular events, underlining the importance of accurate glucometabolic assessment in clinical practice. OBJECTIVE: To investigate different methods to identify glucose disturbances among patients with acute and stable coronary heart disease. METHODS: Consecutive patients referred to cardiologists were prospectively enrolled at 110 centres in 25 countries (n = 4961). Fasting plasma glucose (FPG) and glycaemia 2 h after a 75-g glucose load were requested in patients without known glucose abnormalities (n = 3362). Glucose metabolism was classified according to the World Health Organization and American Diabetes Association (ADA; 1997, 2004) criteria as normal, impaired fasting glucose (IFG), impaired glucose tolerance (IGT) or diabetes. RESULTS: Data on FPG and 2-h post-load glycaemia were available for 1867 patients, of whom 870 (47%) had normal glucose regulation, 87 (5%) had IFG, 591 (32%) had IGT and 319 (17%) had diabetes. If classification had been based on the ADA criterion from 1997, the proportion of misclassified (underdiagnosed) patients would have been 39%. The ADA 2004 criterion would have overdiagnosed 8% and underdiagnosed 33% of the patients, resulting in a total misclassification rate of 41%. For ethical concerns and practical reasons, oral glucose tolerance test (OGTT) was not conducted in 1495 of eligible patients. These patients were more often women, had higher age and waist circumference, and were therefore more likely to have AGR than those who were included. A model based on easily available clinical and laboratory variables, including FPG, high-density lipoprotein cholesterol, age and the logarithm of glycated haemoglobin A1c, misclassified 44% of the patients, of whom 18% were overdiagnosed and 26% were underdiagnosed. CONCLUSION: An OGTT is still the most appropriate method for the clinical assessment of glucometabolic status in patients with coronary heart disease.

Thirty day prognosis of patients with acute pulmonary oedema complicating acute coronary syndromes.

OBJECTIVES: To investigate the characteristics of the acute coronary syndromes underlying acute pulmonary oedema and their 30 day prognosis. PATIENTS: 185 consecutive patients with acute coronary syndromes and acute pulmonary oedema admitted to a tertiary care centre. MAIN OUTCOME AND MEASURES: Clinical, ECG, echocardiographic, enzymatic, and angiographic features were prospectively investigated. RESULTS: Non-ST segment elevation myocardial infarction (NSTEMI) was the most frequent cause of acute pulmonary oedema (61%) followed by unstable angina (UA; 21%) and ST segment elevation myocardial infarction (STEMI; 18%). In each group, mean age was > or = 70 years, but NSTEMI patients were the oldest and > or = 65% of patients had chronic hypertension. Moreover, patients with NSTEMI and UA were older and had a higher incidence of diabetes, previous myocardial infarction, and moderate to severe mitral regurgitation but a similarly reduced ejection fraction (NSTEMI, 41%; UA, 39%; and STEMI, 39%) and increased incidence of diastolic dysfunction and rate of multivessel disease (94%, 87%, and 86%, respectively). However, patients with STEMI had a higher creatine kinase MB peak concentration (158 v 76 microg/l in the NSTEMI group, p < 0.001) and 30 day mortality (26% v 9% in the NSTEMI group and 8% in the UA group, p < 0.024). Multivariate analysis identified ejection fraction < 40% and a peak creatine kinase MB concentration > 100 microg/l as the main prognostic markers (p < 0.03). CONCLUSIONS: Acute pulmonary oedema is mostly a complication of elderly hypertensive patients with NSTEMI or UA (82%) and with multivessel disease often associated with mitral regurgitation. On the other hand, the larger infarct size and higher mortality in patients with STEMI with a similarly reduced ejection fraction suggest a more extensive acute systolic loss.

Usefulness of myocardial perfusion SPECT in patients with left bundle branch block and previous myocardial infarction.

BACKGROUND: The diagnostic value of myocardial perfusion scintigraphy in patients with left bundle branch block (LBBB) and previous acute myocardial infarction has not been evaluated. OBJECTIVE: To determine the utility of single photon emission computed tomography (SPECT) in patients with LBBB and previous acute myocardial infarction. METHODS: Seventy two consecutive patients with permanent LBBB and previous acute myocardial infarction were studied with stress-rest SPECT using 99mTc compounds. The same stress procedures were followed in all patients: (1) exercise alone when it was sufficient; (2) exercise plus simultaneous administration of dipyridamole if exercise was insufficient. RESULTS: In 26 of 28 patients (93%) who had a Q wave acute myocardial infarct before the development of LBBB, there was concordance between abnormal Q waves and rest SPECT in the localisation of myocardial necrosis (kappa = 0.836; p = 0.0001). In 48 patients who had coronary angiography, the positive predictive value of exercise (+dipyridamole) myocardial SPECT for the diagnosis of left anterior descending coronary artery stenosis was 93%, for left circumflex coronary artery stenosis, 96%, and for right coronary artery stenosis, 89%. Specificity values were 83%, 91%, and 69%, respectively. However, sensitivity (69%, 64%, and 89%) and negative predictive values (48%, 46%, and 82%) were suboptimal. CONCLUSIONS: Rest myocardial perfusion SPECT with technetium compounds is useful for localising healed myocardial infarction in patients with LBBB, and exercise (+dipyridamole) SPECT has a high positive predictive value and specificity for the diagnosis of coronary stenosis in these patients.

Experience with enoxaparin in patients with mechanical heart valves who must withhold acenocumarol.

OBJECTIVES: To evaluate the incidence of thromboembolic and haemorrhagic events in a cohort of patients with mechanical heart valves who had to withhold acenocumarol and were treated with enoxaparin. DESIGN: Observational prospective study. SETTING: In hospital; after discharge, and follow up by telephone call. PATIENTS AND METHODS: All consecutive patients with mechanical heart valves admitted to the authors' hospital between May 1999 and January 2002 who had to interrupt treatment with acenocumarol and were treated with enoxaparin as an alternative to other methods were enrolled. In each patient, the following characteristics were prospectively determined: the reason for interrupting acenocumarol, demographic data, estimated global risk for thromboembolic events, international normalised ratio before starting enoxaparin treatment, number of days taking enoxaparin, and mean level of anti-Xa activity during treatment. All patients were followed up through clinical history during the hospitalisation and by telephone after discharge to detect thromboembolic events. MAIN OUTCOME MEASURE: Presence of thromboembolic or haemorrhagic events. RESULTS: 82 patients were identified and followed up for a mean of 2.8 months (range 1.5-3.5 months) after discharge. 61 of them (74%) had one or more associated thromboembolic risk factors. Acenocumarol was interrupted (to perform an invasive procedure in 74 patients and because of haemorrhagic complication in 8) an average of 11.2 days (range 3-40 days). Most patients received the standard enoxaparin dose (1 mg/kg at 12 hour intervals). Mean (SD) anti-Xa activity was 0.58 (0.3) IU/ml (median 0.51). There were 8 minor and 1 major bleeding events during enoxaparin treatment. No thromboembolic complications were clinically detected during hospitalisation or during follow up (95% confidence interval 0% to 3.6%). CONCLUSIONS: Enoxaparin may be an effective and relatively safe substitute anticoagulant for patients with mechanical heart valves who must withhold acenocumarol.

Intravascular ultrasound of the elastic pulmonary arteries: a new approach for the evaluation of primary pulmonary hypertension.

OBJECTIVE: To assess the structural and functional characteristics of pulmonary arteries by intravascular ultrasound (IVUS) in the setting of primary pulmonary hypertension, and to correlate the ultrasound findings with haemodynamic variables and mortality at follow up. DESIGN: Prospective observational study. SETTING: University hospital (tertiary referral centre). PATIENTS: 20 consecutive patients with primary pulmonary hypertension (16 female; mean (SD) age, 39 (14) years). METHODS: Cardiac catheterisation and simultaneous IVUS of pulmonary artery branches at baseline and after infusion of epoprostenol. RESULTS: 33 pulmonary arteries with a mean diameter of 3.91 (0.80) mm were imaged, and wall thickening was observed in all cases, 64% being eccentric. Mean wall thickness was 0.37 (0.13) mm, percentage wall area 31.0 (9.3)%, pulsatility 14.6 (4.8)%, and pulmonary/elastic strain index 449 (174) mm Hg. No correlation was observed between IVUS findings and haemodynamic variables. Epoprostenol infusion increased pulsatility by 53% and decreased the pulmonary/elastic strain index by 41% (p = 0.0001), irrespective of haemodynamic changes. At 18 (12) months follow up, nine patients had died. A reduced pulsatility and an increased pulmonary/elastic strain index were associated with increased mortality at follow up (12.0 (4.4)% v 16.4 (4.4)%, p = 0.03; 369 (67) v 546 (216) mm Hg, p = 0.02). CONCLUSIONS: IVUS demonstrated pulmonary artery wall abnormalities in all patients with primary pulmonary hypertension, mostly eccentric. The severity of the changes did not correlate with haemodynamic variables, and epoprostenol improved pulmonary vessel stiffness. There was an association between impaired pulmonary artery functional state as determined by IVUS and mortality at follow up.

Reproducibility of sequential head-up tilt testing in patients with recent syncope, normal ECG and no structural heart disease.

AIMS: To assess the reproducibility of the response to sequential head-up tilt tests. METHODS AND RESULTS: A head-up tilt test was performed early after syncope in 127 patients with a normal ECG and no structural heart disease. Patients with a positive response (82 patients) were randomized to two (1 week and 2 weeks later) or one (2 weeks later) additional head-up tilt tests, and patients with a negative response (45 patients) were randomized to a second head-up tilt test 1 or 2 weeks after the first. The reproducibility of a positive response in the second head-up tilt test was 80% after 1 week and 53% after 2 weeks (P<0.01). Only 53% of the patients with a positive response to a first and second head-up tilt test had a positive response to a third (P=0.01). Intra-individual variation in the time to a positive response was wide. The reproducibility of the cardioinhibitory responses was very poor. Reproducibility of a negative response was 80%. CONCLUSIONS: In patients with recent syncope, the rate of positive responses decreases with sequential head-up tilt tests. Furthermore, the time to a positive response in different head-up tilt tests shows important intra-individual variations, and the reproducibility of the cardioinhibitory responses is very poor. In contrast, the reproducibility of the negative responses is high.

Frequency and clinical significance of myocardial ischemia detected early after coronary stent implantation.

UNLABELLED: A high number (30%-50%) of reversible defects have been detected early after coronary balloon angioplasty. Inadequate luminal enlargement despite a good angiographic appearance has been suggested as a possible mechanism of these perfusion abnormalities, and some reports have shown better coronary flow reserve after coronary stent implantation than after balloon dilatation. The primary objective of this study was to evaluate the frequency of early ischemic defects detected by maximal exercise (plus dipyridamole) with (99m)Tc-tetrofosmin SPECT after successful coronary angioplasty with stent implantation. A secondary objective was to determine the prognostic value of these early ischemic defects. METHODS: Thirty patients without previous myocardial infarction who successfully underwent 1-vessel coronary angioplasty with stent implantation were studied. Maximal-exercise (99m)Tc-tetrofosmin myocardial SPECT, with simultaneous dipyridamole if exercise was suboptimal, was performed at 6 +/- 1 d (mean +/- SD) after percutaneous transluminal coronary angioplasty. At 8 +/- 3 mo, all patients were followed up clinically, and 77% of them underwent follow-up angiography. RESULTS: The percentage of stenosis decreased from 68.5% +/- 12.6% of luminal diameter to 9.3% +/- 8.8% after stent implantation, and minimal luminal diameter increased from 0.89 +/- 0.36 mm to 2.85 +/- 0.45 mm. Mild-to-moderate reversible myocardial defects in the territory of the dilated artery were detected in 5 patients (17%), with no angiographic or procedural differences occurring between them and patients without ischemic defects. At follow-up, the target lesion revascularization rates depending on the presence or absence of early ischemic defects were 40% and 8%, respectively (P = 0.18). Angiographic restenosis occurred in 3 of 4 patients who had early ischemic defects and underwent follow-up angiography and in 3 of 19 patients who had no early ischemic defects and underwent follow-up angiography (restenosis rate, 75% and 16%, respectively; P < 0.05). CONCLUSION: Coronary angioplasty with stent implantation is associated with a 17% rate of ischemic defects early after the procedure. Patients with early myocardial perfusion defects after coronary stent implantation had a high rate of restenosis.

[Myocardial perfusion SPECT and isotopic ventriculography in obstructive and non-obstructive hypertrophic myocardiopathy]. / SPET miocárdico de perfusión y ventriculografía isotópica en la miocardiopatía hipertrófica obstructiva y no obstructiva.

OBJECTIVE: To evaluate the role of myocardial perfusion SPET and radionuclide ventriculography in patients with hypertrophic cardiomyopathy (HC). METHODS: Exercise myocardial perfusion SPET with 99mTc-tetrofosmin and radionuclide ventriculography were performed in a consecutive series of 101 patients (54 15 years, 50 women, 55 with dynamic obstruction) diagnosed of HC by echo. Follow-up from the diagnosis was 9,9 6,7 years (1 to 28 years). RESULTS: Thirty six percent of patients had perfusion defects (non reversible in 15 and reversible in 21). In non obstructive HC higher number of patients with non reversible defects (p = 0.01 was obseved and in patients with no reversible defects higher incidence of pathologic Q waves in ECG (p = 0.01), Higher ventricular volumes (p < 0.05), lower ejection fraction (p = 0,0001) and longer time to peak emptying velocity (p < 0.05). There were 4 cardiac deaths, 15 syncopes, 18 pacemakers and 6 myectomy. Ejection fraction was higher in patients with syncope (p = 0,034) and there was no isotopic variable predictive of mortality, pacemaker or myectomy. CONCLUSIONS: Neither SPET nor radionuclide ventriculography have a prognostic role in patients with HC, but patients with syncope have higher values of ejection fraction. Patients with non reversible defects have higher rate of pathologic Q waves in ECG, higher ventricular volumes and lower ejection fraction. This is indicative of evolution to dilated form of HC.

Practical recommendations for the use of ACE inhibitors, beta-blockers and spironolactone in heart failure: putting guidelines into practice.

Surveys of prescribing in both hospitals and primary care have shown delays in translating improved survival data from clinical trials into clinical practice thereby denying patients the benefits of proven treatments, such as the angiotensin converting enzyme inhibitors. This may be due to unfamiliarity with clinical guidelines and concerns about adverse events. Recent trials have shown that substantial improvements in survival are associated with spironolactone and beta-blocker therapy. In order to accelerate the uptake of these treatments, and to ensure that all eligible patients should receive the most appropriate medications, a clear and concise set of clinical recommendations has been prepared by a group of clinicians with practical expertise in the management of heart failure. The objective of these recommendations is to provide practical guidance for non-specialists in order to support the implementation of evidenced-based therapy for heart failure. These practical recommendations are meant to supplement rather than replace existing guidelines.

Standard provocative manoeuvres in patients with and without left bundle branch block studied with myocardial SPECT.

BACKGROUND: The objective of this study was to determine the prevalence of anterior and septal defects in patients with left bundle branch block (LBBB), and to assess the diagnostic accuracy of myocardial single photon emission computed tomography (SPECT) with technetium compounds in patients with and without LBBB using standard provocative manoeuvres. METHODS: Five hundred and nine consecutive patients (456 without LBBB and 53 with LBBB) without previous infarction who had a coronary angiography performed within <3 months of the scintigraphic study were retrospectively evaluated. The same stress procedures were followed in all patients. (1) Only exercise when it was sufficient; and (2) exercise + simultaneous administration of dypiridamole if exercise was insufficient. Only reversible defects were considered positive and > or =50% of coronary stenosis was considered significant. RESULTS: Prevalence of reversible anterior and septal defects was low (33% and 12%, respectively) in patients with LBBB. Although lower values of global sensitivity (81%) and specificity (73%) were obtained in these patients, there were no significant differences with respect to the patients without LBBB (89% and 86%, respectively). Specificity values for the diagnosis of stenosis of left anterior descending (78%), left circumflex (96%) and right coronary artery (74%) in patients with LBBB were lower, but without significant statistical differences with respect patients without LBBB (90%, 96% and 82%, respectively). CONCLUSIONS: Myocardial SPECT with technetium compounds, using standard provocation manoeuvres, can be used in patients with LBBB with only a mild decrease in diagnostic accuracy as compared to patients without LBBB.

Intravenous administration of the natriuretic peptide urodilatin at low doses during coronary reperfusion limits infarct size in anesthetized pigs.

OBJECTIVE: It has been shown that cGMP content is reduced in post-ischemic myocardium, and that stimulation of cGMP synthesis prevents cardiomyocyte hypercontracture and cell death in vitro. This study was aimed at determining whether administration of the natriuretic peptide urodilatin (URO) at the time of reperfusion could limit myocardial cell death secondary to transient coronary occlusion. METHODS: The relation between cGMP content in reperfused myocardium and the extent of cell death was investigated in isolated rat hearts (n=62) receiving different URO concentrations during initial reperfusion. The dose of intravenous URO necessary to obtain the targeted increase in cGMP in reperfused myocardium was investigated in ten pigs submitted to transient coronary occlusion (CO), and the effect of two selected doses of URO on infarct size was investigated in 22 pigs. RESULTS: cGMP was severely reduced in post-ischemic rat hearts. Addition of 0.01 microM URO during the first 15 min of reperfusion had no effect on myocardial cGMP content, functional recovery or LDH release in hearts submitted to 40 or 60 min of ischemia. At 0.05 microM, URO increased myocardial cGMP to 111% of values in normoxic hearts, improved functional recovery (P=0.01) and reduced peak LDH released by 40% (P=0.02). The beneficial effect of urodilatin was abolished by ANP receptor inhibition. At 1 microM, URO increased cGMP in reperfused myocardium to 363% of normoxic controls and had no beneficial effect. In pigs allocated to 47 min of CO and 5 min of reperfusion, cGMP was markedly reduced in reperfused myocardium. Intravenous URO at 10 ng/kg per min during the first 25 min of reperfusion normalized myocardial cGMP after 5 min of reflow (95% of control myocardium), and reduced infarct size by 40% (P=0.04). At 50 ng/kg per min, urodilatin increased myocardial cGMP in reperfused myocardium to 335% of control myocardium and failed to significantly reduce infarct size (46 vs. 66%, P=0.125). None of these doses had detectable hemodynamic effects. CONCLUSIONS: Intravenous low-dose URO at the time of reperfusion normalizes myocardial cGMP and limits necrosis. Large doses of URO increasing myocardial cGMP well over normal values may lack this beneficial effect.

Survival following self-limited left ventricular free wall rupture during myocardial infarction. Management differences between patients with or without pseudoaneurysm formation.

The clinical, angiographic and therapeutic features of eight patients who developed a left ventricular pseudoaneurysm (PA) after an acute myocardial infarction (AMI) and those of 25 who did not develop this complication following a medically managed left ventricular free wall rupture (FWR) were compared. These 25 patients were treated with pericardiocentesis, extended rest and strict blood pressure control. Most patients with FWR or PA had a first AMI and absence of overt heart failure. Both groups had a comparable age, frequency of systemic hypertension and extent of coronary disease. Pericardial effusion (> or =10 mm) was documented in all patients with FWR and in two of the three with PA with this information. Twenty four patients with FWR were hospitalized within the first 48 h (96%) but only three of those with PA (37.5%, P<0.002). Moreover, in patients with PA, a FWR was not suspected during AMI and, as opposed to those with FWR, they did not undergo a strict blood pressure control or a restriction of physical activity following AMI. Also, beta blockers were administered to 15 patients with FWR (60%) but to only one with PA (11%, P<0.02). Our findings suggest that failure to recognise a self limited FWR during AMI and to provide adequate control of blood pressure and physical exercise during the acute phase and the early weeks postinfarction, are likely to favor development of PA.

Long term results of mechanical prostheses for treatment of active infective endocarditis.

OBJECTIVE: To analyse the long term results of mechanical prostheses for treating active infective endocarditis. DESIGN: Prospective cohort study of a consecutive series of patients diagnosed with infective endocarditis and operated on in the active phase of the infection for insertion of a mechanical prosthesis. SETTING: Tertiary referral centre in a metropolitan area. RESULTS: Between 1975 and 1997, 637 cases of infective endocarditis were diagnosed in the centre. Of these, 436 were left sided (with overall mortality of 20.3%). Surgical treatment in the active phase of the infection was needed in 141 patients (72% native, 28% prosthetic infective endocarditis). Mechanical prostheses were used in 131 patients. Operative mortality was 30.5% (40 patients). Ninety one survivors were followed up prospectively for (mean (SD)) 5.4 (4.5) years. Thirteen patients developed prosthetic valve dysfunction. Nine patients suffered reinfection: four of these (4%) were early and five were late. The median time from surgery for late reinfection was 1.4 years. During follow up, 12 patients died. Excluding operative mortality, actuarial survival was 86.6% at five years and 83.7% at 10 years; actuarial survival free from death, reoperation, and reinfection was 73.1% at five years and 59.8% at 10 years. CONCLUSIONS: In patients surviving acute infective endocarditis and receiving mechanical prostheses, the rate of early reinfection compares well with reported results of homografts. In addition, prosthesis dysfunction rate is low and long term survival is good. These data should prove useful for comparison with long term studies, when available, using other types of valve surgery in active infective endocarditis.

Relationship between the location of the most severe myocardial perfusion defects, the most severe coronary artery stenosis, and the site of subsequent myocardial infarction.

UNLABELLED: This study evaluated the relationship between the location of the most severe myocardial perfusion defects, the most severe coronary artery stenosis, and the site of subsequent acute myocardial infarction (AMI). METHODS: Of 3,180 patients who were admitted with a diagnosis of AMI, we identified 44 patients who had undergone previous myocardial perfusion SPECT. Thirty-one of them also had previous coronary angiography. The relationship between the location of the myocardial perfusion defects, the coronary artery stenosis, and the site of subsequent AMI was studied in these patients. RESULTS: The concordance between the location of the most severe reversible defects detected by SPECT and the site of subsequent AMI was 71% (kappa = 0.499). The concordance between the most severe stenosis detected by coronary angiography and the site of subsequent AMI was 64% (kappa = 0.451). However, kappa values for SPECT and coronary angiography were good when the interval between these investigations and subsequent AMI was <3 mo (0.724 and 0.661, respectively), for moderate to severe perfusion defects (0.719), and for 90%-99% coronary stenosis (0.626). CONCLUSION: The culprit lesion is not always the one that is manifested by the most severe reversible perfusion defect or the most critical coronary artery stenosis. Myocardial SPECT and coronary angiography can predict the location of a future AMI in 71% and 64% of patients, respectively. The percentage is higher when the interval between investigations and subsequent AMI is <3 mo, for moderate to severe perfusion defects, and for 90%-99% coronary stenosis.

Variations in diagnostic yield of head-up tilt test and electrophysiology in groups of patients with syncope of unknown origin.

AIMS: To assess the diagnostic yield of the head-up tilt test and electrophysiology in different groups of patients with syncope of unknown origin established according to simple clinical criteria. METHODS AND RESULTS: Six hundred consecutive patients with syncope of unknown origin submitted to a tilt test. Two hundred and forty seven of them also underwent electrophysiology. Patients were divided into groups according to age at the time of first syncope, ECG findings and the presence of organic heart disease. Positive responses to the tilt test were more common in patients who had suffered their first syncope at an age equal to or below 65 years (group I) than in older patients (group II) (47% vs 33%, P<0.05, OR 1.8, CI 1.2-2.78), and in patients with a normal ECG and without organic heart disease than in the other subgroups of patients (47% vs 37%, P<0.008, OR 1.6). The lowest rate of positive response was observed in older patients with an abnormal ECG and organic heart disease. Electrophysiology disclosed abnormal findings in group II more often than in group I (23% vs 7%, P<0.001, OR 3.7, CI 1.7-9.2). The diagnostic yield from electrophysiology was higher in patients with an abnormal ECG than in those with a normal ECG (22% vs 3.7%, P<0.0005, OR 7.1), and it was especially low in patients with a normal ECG and without organic heart disease (2.6%). CONCLUSION: The diagnostic yield of the tilt test and electrophysiology differs in groups of patients with syncope of unknown origin, established according to simple clinical criteria. These findings have a bearing on selecting the most appropriate test in a particular patient.

Persistence of gap junction communication during myocardial ischemia.

During myocardial ischemia, severe ATP depletion induces rigor contracture followed by intracellular Ca2+ concentration ([Ca2+]i) rise and progressive impairment of gap junction (GJ)-mediated electrical coupling. Our objective was to investigate whether chemical coupling through GJ allows propagation of rigor in cardiomyocytes and whether it persists after rigor development. In end-to-end connected adult rat cardiomyocytes submitted to simulated ischemia the interval between rigor onset was 3.7 +/- 0.7 s, and subsequent [Ca2+]i rise was virtually identical in both cells, whereas in nonconnected cell pairs the interval was 71 +/- 12 s and the rate of [Ca2+]i rise was highly variable. The GJ blocker 18alpha-glycyrrhetinic acid increased the interval between rigor onset and the differences in [Ca(2+)]i between connected cells. Transfer of Lucifer yellow demonstrated GJ permeability 10 min after rigor onset in connected cell pairs, and 30 min after rigor onset in isolated rat hearts submitted to nonflow ischemia but was abolished after 2 h of ischemia. GJ-mediated communication allows propagation of rigor in ischemic myocytes and persists after rigor development despite acidosis and increased [Ca2+]i.

[Prognostic value of cardiac perfusion scintigraphy associated with the dobutamine test in acute coronary syndromes]. / Valor pronóstico de la gammagrafía cardíaca de perfusión asociada al test de dobutamina en los síndromes coronarios agudos.

OBJECTIVES: This study aimed to establish the value of myocardial ischemia induced by the dobutamine infusion test associated to 99m technetium isonitrile single photon emission computed tomography in patients with unstable angina or non Q-wave infarction during the first days in the Coronary Care Unit. METHODS: Fifty three patients with unstable coronary syndromes and common medical treatment were studied with a moderate-dose dobutamine test (5 to 20 microgram/Kg/min) using a 99mTc-MIBI SPECT. The results were correlated with the incidence of recurrent angina, infarction, death or revascularization. RESULTS: The dobutamine test induced a reversible perfusion defect in 36 patients (68%) and angina in 12 of them (12/36, 33%). However, the patients who had a positive test had a similar incidence of events as those with a negative test (58% vs 59%). Thus, while the sensitivity of the dobutamine test to identify patients at risk was relatively high (68%), its specificity (32%) and its negative predictive value (41%) were low. The patients with dobutamine-induced angina, however, had a higher scintigraphy score (3.0 +/- 1,7 vs 1.6 +/- 1.8, p < 0.02) and a higher incidence of recurrent angina (8/12, 67% vs 13/41, 31%, p < 0.04) than those without, at a comparable double product. CONCLUSIONS: In conventionally treated patients with unstable coronary syndromes, the specificity of the inducible scintigraphic ischemia with moderate dose of dobutamine performed during the first days is too low to be used as a marker for in-hospital events. However, inducible angina with dobutamine suggests an extensive jeopardized area and/or a particularly reduced ischemic threshold.