Impact of the 2005 and 2010 Spanish smoking laws on hospital admissions for tobacco-related diseases in Valencia, Spain.

OBJECTIVES: This study aimed to assess the impact of the latest smoke-free legislation on hospital admission rates due to smoking-related diseases in Spain. STUDY DESIGN: A retrospective cohort study was conducted to evaluate changes in hospital admission rates for cardiovascular, respiratory diseases, and smoking-related cancer in Valencia, Spain, during the period 1995-2013. Law 28/2005 and then law 42/2010 prohibited smoking in bars and restaurants as well as playgrounds and access points to schools and hospitals. METHODS: General population data by age and sex were obtained from the National Institute of Statistics census. Data on hospital admissions were obtained from the Minimum Basic Data Set. Diagnoses were codified according to the International Classification of Diseases-9th revision. Data from all hospitals of the Valencian Community from 1995 to 2013 were analysed. Trend analyses in the periods before and after the approval of the 2005 law were conducted using least-squares linear regression models. RESULTS: Adjusted hospital admission rates per 100,000 inhabitants for cardiovascular diseases significantly decreased after the 2005 Law (from 550.0/100,000 in 2005 to 500.5/100,000 in 2007), with a further decrease (to 434.6/100,000) in 2013, after the 2010 Law. Reductions in hospital admissions were seen in men and women, although declining trends were more marked in men. Hospital admission rates for respiratory diseases showed a reduction of a lower magnitude, whereas for smoking-related cancer admissions there was a slight decline only among men. CONCLUSIONS: The Spanish comprehensive smoking ban resulted in a remarkable reduction of the adjusted rate of hospital admissions mainly associated to cardiovascular diseases. The decrease in the number of persons requiring in-patient care is relevant and may be viewed as an improvement of the public's health.

A quantitative structural and morphometric analysis of the Purkinje network and the Purkinje-myocardial junctions in pig hearts.

The morpho-functional properties of the distal section of the cardiac Purkinje network (PN) and the Purkinje-myocardial junctions (PMJs) are fundamental to understanding the sequence of electrical activation in the heart. The overall structure of the system has already been described, and several computational models have been developed to gain insight into its involvement in cardiac arrhythmias or its interaction with implantable devices, such as pacemakers. However, anatomical descriptions of the PN in the literature have not enabled enough improvements in the accuracy of anatomical-based electrophysiological simulations of the PN in 3D hearts models. In this work, we study the global distribution and morphological properties of the PN, with special emphasis on the cellular and architectural characterization of its intramural branching structure, mesh-like sub-endocardial network, and the PMJs in adult pig hearts by both histopathological and morphometric evaluation. We have defined three main patterns of PMJ: contact through cell bodies, contact through cell prolongations either thick or piliform, and contact through transitional cells. Moreover, from hundreds of micrographs, we quantified the density of PMJs and provided data for the basal/medial/apical regions, anterior/posterior/septal/lateral regions and myocardial/sub-endocardial distribution. Morphometric variables, such as Purkinje cell density and thickness of the bundles, were also analyzed. After combining the results of these parameters, a different septoanterior distribution in the Purkinje cell density was observed towards the cardiac apex, which is associated with a progressive thinning of the conduction bundles and the posterolateral ascension of intramyocardial terminal scattered fibers. The study of the PMJs revealed a decreasing trend towards the base that may anatomically explain the early apical activation. The anterolateral region contains the greatest number of contacts, followed by the anterior and septal regions. This supports the hypothesis that thin distal Purkinje bundles create a junction-rich network that may be responsible for the quick apical depolarization. The PN then ascends laterally and spreads through the anterior and medial walls up to the base. We have established the first morphometric study of the Purkinje system, and provided quantitative and objective data that facilitate its incorporation into the development of models beyond gross and variable pathological descriptions, and which, after further studies, could be useful in the characterization of pathological processes or therapeutic procedures.

Modifications of long-term heart rate variability produced in an experimental model of diet-induced metabolic syndrome.

Metabolic syndrome (MetS) has been linked to a higher prevalence of cardiac arrhythmias, the most frequent being atrial fibrillation, but the mechanisms are not well understood. One possible underlying mechanism may be an abnormal modulation of autonomic nervous system activity, which can be quantified by analysing heart rate variability (HRV). Our aim was to investigate the modifications of long-term HRV in an experimental model of diet-induced MetS to identify the early changes in HRV and the link between autonomic dysregulation and MetS components. NZW rabbits were randomly assigned to control (n = 10) or MetS (n = 10) groups, fed 28 weeks with high-fat, high-sucrose diet. 24-hour recordings were used to analyse HRV at week 28 using time-domain, frequency-domain and nonlinear analyses. Time-domain analysis showed a decrease in RR interval and triangular index (Ti). In the frequency domain, we found a decrease in the low frequency band. Nonlinear analyses showed a decrease in DFA-α1 and DFA-α2 (detrended fluctuations analysis) and maximum multiscale entropy. The strongest association between HRV parameters and markers of MetS was found between Ti and mean arterial pressure, and Ti and left atrial diameter, which could point towards the initial changes induced by the autonomic imbalance in MetS.

The training-induced changes on automatism, conduction and myocardial refractoriness are not mediated by parasympathetic postganglionic neurons activity.

The purpose of this study is to test the role that parasympathetic postganglionic neurons could play on the adaptive electrophysiological changes produced by physical training on intrinsic myocardial automatism, conduction and refractoriness. Trained rabbits were submitted to a physical training protocol on treadmill during 6 weeks. The electrophysiological study was performed in an isolated heart preparation. The investigated myocardial properties were: (a) sinus automatism, (b) atrioventricular and ventriculoatrial conduction, (c) atrial, conduction system and ventricular refractoriness. The parameters to study the refractoriness were obtained by means of extrastimulus test at four different pacing cycle lengths (10% shorter than spontaneous sinus cycle length, 250, 200 and 150 ms) and (d) mean dominant frequency (DF) of the induced ventricular fibrillation (VF), using a spectral method. The electrophysiological protocol was performed before and during continuous atropine administration (1 µM), in order to block cholinergic receptors. Cholinergic receptor blockade did not modify either the increase in sinus cycle length, atrioventricular conduction and refractoriness (left ventricular and atrioventricular conduction system functional refractory periods) or the decrease of DF of VF. These findings reveal that the myocardial electrophysiological modifications produced by physical training are not mediated by intrinsic cardiac parasympathetic activity.

High-sensitivity troponin T and the risk of recurrent readmissions after hospitalisation for acute heart failure. / Troponina T de alta sensibilidad y riesgo de hospitalizaciones recurrentes tras un ingreso por insuficiencia cardíaca aguda.

OBJECTIVES: High-sensitivity troponin is a biomarker of myocardial damage and is associated with a greater risk of mortality and disease progression in patients with acute heart failure (AHF). However, its relationship with the risk of future readmissions is less known. The aim of this study was to assess the association between ultrasensitive troponin T (TnT-us) values in patients with AHF and the risk of recurrent readmissions in the follow-up. METHODS: We prospectively included a cohort of 621 consecutive patients with AHF, excluding those patients with acute coronary syndrome. We measured the TnT-us levels obtained during the first medical contact in the emergency department. The risk of cumulative readmissions was assessed using negative binomial regression. RESULTS: The mean age of the participants was 73.6±10.8 years, 54.6% were men, and 52% had a left ventricular systolic function ≥50%. The median TnT-us level was 35.5pg/ml (interquartile range [IQR], 22-67). After a median follow-up of 1.2 years (IQR, 0.4-2.4), a total of 153 deaths (24.6%) were recorded, as well as 689 readmissions for all causes in 303 patients (48.8%) and 286 readmissions for HF in 163 patients (26.3%). In the multivariate analysis, the high TnT-us values were associated with an increased risk of readmission, both for all causes and for HF (incidence rate ratio [IRR], 1.16; 95% confidence interval, 1.02-1.36; p=.029 and IRR, 1.23; 95% confidence interval, 1.04-1.46; p=.018, respectively). CONCLUSIONS: For patients with AHF, the increase in TnT-us levels was independently associated with a risk of recurrent readmissions during the follow-up.

Alteration of ventricular fibrillation by flecainide, verapamil, and sotalol: an experimental study.

BACKGROUND: The purpose of this study was to determine whether the myocardial electrophysiological properties are useful for predicting changes in the ventricular fibrillatory pattern. METHODS AND RESULTS: Thirty-two Langendorff-perfused rabbit hearts were used to record ventricular fibrillatory activity with an epicardial multiple electrode. Under control conditions and after flecainide, verapamil, or d,l-sotalol, the dominant frequency (FrD), type of activation maps, conduction velocity, functional refractory period, and wavelength (WL) of excitation were determined during ventricular fibrillation (VF). Flecainide (1.9+/-0.3 versus 2.4+/-0.6 cm, P<0. 05) and sotalol (2.1+/-0.3 versus 2.5+/-0.5 cm, P<0.05) prolonged WL and diminished FrD during VF, whereas verapamil (2.0+/-0.2 versus 1. 7+/-0.2 cm, P<0.001) shortened WL and increased FrD. Simple linear regression revealed an inverse relation between FrD and the functional refractory period (r=0.66, P<0.0001), a direct relation with respect to conduction velocity (r=0.33, P<0.01), and an inverse relation with respect to WL estimated during VF (r=0.49, P<0.0001). By stepwise multiple regression, the functional refractory periods were the only predictors of FrD. Flecainide and sotalol increased the circuit size of the reentrant activations, whereas verapamil decreased it. The 3 drugs significantly reduced the percentages of more complex activation maps during VF. CONCLUSIONS: The activation frequency is inversely related to WL during VF, although a closer relation is observed with the functional refractory period. Despite the diverging effects of verapamil versus flecainide and sotalol on the activation frequency, WL, and size of the reentrant circuits, all 3 drugs reduce activation pattern complexity during VF.

Low-dose dobutamine testing using contrast left ventriculography in the same session as coronary angiography predicts the improvement of left ventricular function after coronary angioplasty in postinfarction patients.

The role of percutaneous transluminal coronary angioplasty (PTCA) in the subacute or chronic phases of myocardial infarction remains controversial. This study investigates the usefulness of dobutamine contrast left ventriculography in a single session with coronary angiography for predicting the improvement of ventricular function after PTCA. The study group consisted of 30 patients in whom a contrast left ventricular angiogram and PTCA were performed after a first myocardial infarction. The centerline method was used to calculate dysfunction extent at baseline and its variation during dobutamine infusion at 7.5 microg/kg/min; contractile reserve was defined as a significant (> or = 15%) reduction of dysfunction extent. A second ventricular angiogram was performed 6 months later in all patients. Abnormal wall motion extent decreased at 6 months after PTCA (84+/-21% vs 70+/-29%, p = 0.0001). Wall motion improvement after PTCA correlated with the response to dobutamine (r = 0.54, p = 0.002). Ten patients showed a significant reduction (> or = 15%) of dysfunction extent at 6 months; dobutamine testing had a 80% sensitivity, 84% specificity, 67% positive predictive value, and 89% negative predictive value in detecting regional function improvement. In the subgroup of 21 patients without restenosis, both the correlation between dysfunction improvement after PTCA and response to dobutamine (r = 0.72, p = 0.0001) and the accuracy of dobutamine testing (sensitivity 88%, specificity 92%, positive predictive value 88%, and negative predictive value 92%) increased. The ejection fraction significantly increased (>5%) after PTCA in 6 patients; dobutamine testing had a 67% sensitivity, 74% specificity, 44% positive predictive value, and 88% negative predictive value in predicting the increase in the ejection fraction. In the subgroup without restenosis the improvement of the ejection fraction correlated with the response to dobutamine (r = 0.63, p = 0.007), and the sensitivity of dobutamine testing was 80%, specificity 83%, positive predictive value 67%, and negative predictive value 91%. In conclusion, dobutamine contrast left ventriculography testing in the same session as coronary angiography predicts regional function and ejection fraction improvement after PTCA in postinfarction patients, particularly when restenosis does not develop.

Intrinsic changes on automatism, conduction, and refractoriness by exercise in isolated rabbit heart.

We have studied the intrinsic modifications on myocardial automatism, conduction, and refractoriness produced by chronic exercise. Experiments were performed on isolated rabbit hearts. Trained animals were submitted to exercise on a treadmill. The parameters investigated were 1) R-R interval, noncorrected and corrected sinus node recovery time (SNRT) as automatism index; 2) sinoatrial conduction time; 3) Wenckebach cycle length (WCL) and retrograde WCL, as atrioventricular (A-V) and ventriculoatrial conduction index; and 4) effective and functional refractory periods of left ventricle, A-V node, and ventriculoatrial retrograde conduction system. Measurements were also performed on coronary flow, weight of the hearts, and thiobarbituric acid reagent substances and glutathione in myocardium, quadriceps femoris muscle, liver, and kidney, to analyze whether these substances related to oxidative stress were modified by training. The following parameters were larger (P < 0.05) in trained vs. untrained animals: R-R interval (365 +/- 49 vs. 286 +/- 60 ms), WCL (177 +/- 20 vs. 146 +/- 32 ms), and functional refractory period of the left ventricle (172 +/- 27 vs. 141 +/- 5 ms). Corrected SNRT was not different between groups despite the larger noncorrected SNRT obtained in trained animals. Thus training depresses sinus chronotropism, A-V nodal conduction, and increases ventricular refractoriness by intrinsic mechanisms, which do not involve changes in myocardial mass and/or coronary flow.

Role of infarction artery status in left ventricular remodeling after acute myocardial infarction.

The aim of this study was to evaluate the relation between the infarction artery status and left ventricular volumes, independently of regional ventricular dysfunction, at 4-6 weeks after a first myocardial infarction. The study group consisted of 100 patients, of whom 80 received thrombolytic treatment. Coronary and contrast left ventricular angiograms were performed at 36+/-5 days postinfarction. Left ventricular end-diastolic and end-systolic volumes were measured. The centerline chord motion method was used to calculate the extent of wall motion abnormality (percentage of chords with hypokinetic motion) and its severity (maximum units of S.D. below the normal wall motion reference). Minimum lumen diameter, patency and collateral flow in the infarction artery were also analyzed. Eight patients (group I) showed occlusion with poor collateral flow in the infarction artery, 22 patients (group II) occlusion with good collateral flow, 38 patients (group III) severe residual stenosis (minimum lumen diameter < or = 1 mm), and 32 patients (group IV) non-severe residual stenosis (minimum lumen diameter > 1 mm). Patients from group I presented greater wall motion abnormality in terms of both extent (P=0.005) and severity (P=0.007), and greater end-diastolic (P=0.07) and end-systolic (P=0.0008) volumes; there were no differences among groups II, III and IV. By stepwise multivariate regression analysis, the extent of wall motion abnormality was the main determinant of end-diastolic (P=0.0001) and end-systolic (P=0.0001) volumes; occlusion with poor collateral flow was also a significant independent factor for end-systolic volume (P=0.03). Total occlusion (including both with and without collaterals) and the minimum lumen diameter did not correlate with end-diastolic and end-systolic volumes. We concluded that (A) the extent of regional dysfunction is the primary determinant of left ventricular volumes at 4-6 weeks postinfarction. (B) The status of the infarction artery is a weak predictor of end-diastolic volume, which is the best descriptor of ventricular remodeling, although occlusion with poor collateral flow is associated to larger end-systolic volume.

Wall motion of noninfarcted myocardium. Relationship to regional and global systolic function and to early and late left ventricular dilation.

We studied the wall motion of the noninfarcted area and its role in left ventricular remodeling. The study group consisted of 43 patients with a first Q-wave acute myocardial infarction and single-vessel disease. Cardiac catheterization was performed at the first week, and was repeated six months later. Left ventricular volumes, wall motion at the infarcted and noninfarcted area, ejection fraction and infarction-related artery status were quantified. Hyperkinesia was only found at the first week in 22% of cases, and at the sixth month in 26% of cases. Wall motion at the noninfarcted area correlated with wall motion at the infarcted area (one week: r=0.53 p<0.0001; six months: r=0.52 p=0.01), ejection fraction (one week: r=0.69 p<0.0001; six months: r=0.56 p=0.006), end-diastolic volume (one week: r=-0.48 p=0.002; six months: r=-0.48 p=0.02) and end-systolic volume (one week: r=-0.70 p<0.0001; six months: r=-0.64 p=0.001). The improvement of the noninfarcted area (from the first week to the sixth month) was only related to basal (one week) wall motion in this area (r=-0.58 p=0.003). We conclude that after an intermediate-large infarction, most patients exhibit a normal or hypokinetic noninfarcted area. Patients with a more depressed infarcted area show poorer contractility at the noninfarcted area. area exhibit greater progressive improvement.

Stunned myocardium after thrombolytic treatment. Identification by dobutamine echocardiography and role of the residual stenosis in the infarction artery.

UNLABELLED: The aim of this study was to identify post-thrombolysis stunned myocardium using low dose (10 micrograms/kg/min) dobutamine echocardiography, and to elucidate the role of the residual stenosis in the infarction artery in wall motion recovery. Forty-seven consecutive patients treated with thrombolytic agents for a first non-complicated myocardial infarction were included. An early dobutamine echocardiogram was performed 7 +/- 2 days after thrombolysis to calculate a wall motion score index at baseline and with dobutamine. A late resting echocardiogram 36 +/- 7 days and a coronariography 41 +/- 8 days after thrombolysis were also performed. In 12 patients no baseline regional dysfunction was observed in the early echocardiogram (Group I), whereas 35 patients (Group II) presented regional dysfunction which improved with dobutamine in 11 cases (Group IIA), but not in 24 (Group IIB). Maximum creatine kinase peak was smaller in Group I (458 +/- 162, P < or = 0.01) and in Group IIA (931 +/- 593, P < or = 0.05) than in Group IIB (1547 +/- 886). Late resting echocardiogram was performed in 44 patients: all 12 from Group I, 10 from Group IIA and 22 from Group IIB; all patients from Group I persisted with normal wall motion, while the baseline score index improved in seven patients (70%) from Group IIA vs. three patients (14%) from Group IIB (P < or = 0.01). Quantitative angiographic parameters in the infarction artery failed to differentiate the subgroup of patients in whom wall motion improved in the late echocardiogram. By simple regression, smaller creatine kinase peak (P < or = 0.05) and a positive response to dobutamine in the early echocardiogram (P < or = 0.001) correlated with wall motion recovery, but the minimum lumen diameter in the infarction artery did not correlate; by multiple logistic regression, only a positive response to dobutamine in the early echocardiogram independently predicted late wall motion improvement (P < or = 0.001). CONCLUSIONS: (1) Low dose dobutamine echocardiography early after thrombolytic treatment identifies dysfunctional myocardium with potential late spontaneous improvement (stunned myocardium). (2) Myocardial stunning tends to occur in small infarctions. (3) Late wall motion improvement can occur despite severe residual stenosis in the infarction artery.

ST-segment elevation on Q-leads during exercise in patients with ST-segment elevation at rest after myocardial infarction.

INTRODUCTION: ST-segment elevation on Q-leads after an acute myocardial infarction is related to a greater infarct size. The meaning of a further exercise-induced ST-segment elevation in these patients has not been analyzed. METHOD: Thirty-six patients with ST-segment elevation on Q-leads were studied after a first acute myocardial infarction. Exercise testing and cardiac catheterization were performed at the first week. Left ventricular volumes (ml/m(2)); the extent of abnormal wall motion (AWM: chords); contractile reserve (AWM improvement with low dose dobutamine) and coronary patency in the culprit artery were analyzed. Cardiac catheterization was repeated at the sixth month in 20 patients; systolic recovery (AWM improvement), left ventricular volumes and coronary patency were again evaluated. RESULTS: Patients with exercise-induced ST-segment elevation in two or more Q-leads (n=21) showed lesser contractile reserve (6+/-6 vs. 12+/-7 chords, P=0.01) than patients without exercise-induced ST-segment elevation (n=13). AWM (F=8.1) and absence of exercise-induced ST-segment elevation (F=9.5; positive predictive value: 80%; negative predictive value: 68%) were the only independent predictors of contractile reserve. Nevertheless, this electrocardiographic sign was not related to left ventricular volumes, coronary patency or systolic function and it did not predicted late systolic recovery. CONCLUSIONS: In patients with baseline ST-segment elevation on Q-leads an exercise-induced ST-segment elevation is independently related to a lesser contractile reserve but not to the evolution of volumes or regional dysfunction during the first 6 months post-infarction. Therefore, the clinical value of this sign seems to be limited to the non-invasive detection of myocardial viability during the early post-infarction phase.

QT dispersion within the first 6 months after an acute myocardial infarction: relationship with systolic function, left ventricular volumes, infarct related artery status and clinical outcome.

INTRODUCTION: We analysed QT dispersion within the first 6 months postinfarction, its relationship with the main established risk stratifiers and its clinical value. METHODS AND RESULTS: In 55 patients with a first Q-wave myocardial infarction the 12-lead electrocardiogram was scanned and digitised for analysis of QT dispersion (QT maximum-QT minimum) at first day (72 [61-96] ms), first week (69 [47-90] ms), first month (67 [46-88] ms) and sixth month (47 [40-74] ms; P<0.0001 vs. first day). Cardiac catheterization was performed at first week and at sixth month; QT dispersion was not related to ejection fraction, left ventricular volumes, infarct related artery status or contractile reserve (improvement of the infarcted area with low-dose dobutamine); no relation was found between QT dispersion decrease from first week to sixth month with regional systolic function improvement. Finally, during a mean follow-up period of 35+/-22 months QT dispersion was not independently related to clinical events. CONCLUSION: QT dispersion decreases progressively during the first months after myocardial infarction. These changes should be taken into account to define cut-off values of clinical interest in this phase. This variable does not seem related to the classic prognosis predictors. In a nonselected postinfarction population it has a low clinical value.

Relationships between heart rate variability, functional capacity, and left ventricular function following myocardial infarction: an evaluation after one week and six months.

BACKGROUND: Relationships between heart rate (HR) variability and different prognostic markers such as ejection fraction, functional capacity, and patency of the infarct-related artery, as well as the comparison of their time courses are not fully elucidated. HYPOTHESIS: The aim of study was to assess prospectively the early postinfarction changes in HR variability and its evolution over a period of 6 months: the relationships between HR variability and functional capacity in exercise testing; left ventricular function in cardiac catheterization: status of the infarct-related artery; and the comparison of their time courses. METHODS: In 42 patients with anterior myocardial infarction, a study was made of the early changes in HR variability analyzed by the complex demodulation method, its evolution over a period of 6 months. and the relationships between HR variability and (1) functional capacity in exercise testing, (2) left ventricular function in cardiac catheterization, and (3) status of the infarct-related artery. RESULTS: At 1 week HR variability parameters correlated directly with functional capacity indicators such as METS, percent change in HR from rest to peak exercise (%deltaHR), difference between initial and peak HR (HR range), percent peak theoretical HR (% peak HR), left ventricular ejection fraction (EF), and, inversely, with end-systolic volume (ESV). Stepwise multiple regression analysis to establish HR variability parameters (recorded at 1 week) as related to functional capacity and left ventricular function at 1 week and 6 months postinfarction established the following variables: (1) At 1 week: standard deviation (SD) of the RR cycles in relation to %deltaHR (r = 0.60, p <0.0001), HR range (r = 0.43, p < 0.01), and EF (r = 0.79, p < 0.0001). (2) At 6 months, the sole accepted HR variability parameter was the SD in relation to %deltaHR (r = 0.38, p < 0.05) and HR range (r = 0.45, p < 0.01). No variability parameter was accepted in relation to METS, % peak HR, or ESV. Relationship between EF or ESV and HR variability parameters was not significant when both were evaluated at 6 months. At that time, there was a significant increase in all HR variability parameters among all surviving patients (n = 39), with the exception of the LF/HF ratio and mean RR cycle. The percent increase in HR variability between the first week and 6 months was greater among those patients with the lowest basal EF. No relation was established between HR variability and patency of the infarct-related artery. CONCLUSION: The decrease in HR variability observed following myocardial infarction is associated with a diminished functional capacity and an increased alteration of the EF. This does not affect the recovery of HR variability, which was observed in all surviving patients.

Predictors of early and late ventricular remodeling after acute myocardial infarction.

BACKGROUND: The determinants of the early and late stages of the ventricular remodeling process after infarction are not well defined. HYPOTHESIS: The study was undertaken to evaluate the factors that condition the time course of left ventricular dilation during the first 6 months after infarction. METHODS: The study group consisted of 74 patients with a first intermediate-large (> or = 4 Q waves) acute myocardial infarction. Contrast left ventricular and coronary angiograms were performed at 7 +/- 1 and 175 +/- 25 days after infarction. Left ventricular volumes, regional function and infarction artery status were quantified. Percutaneous transluminal coronary angioplasty (PTCA) was performed in the early angiogram in 31 patients. RESULTS: In the early angiogram, 13 patients showed ventricular remodeling (end-diastolic volume > 90 ml/m2). A larger extent of dysfunction was the only predictor (p < 0.002) of early remodeling. At 6 months, a smaller, early end-diastolic volume (p < 0.0001) and a poorer regional function recovery (p < 0.05) were independently related to late diastolic enlargement, and a poorer regional function recovery (p < 0.0001) and a smaller, early end-systolic volume (p < 0.009) were independently related to late systolic enlargement. One patient with compared with 20 patients without early remodeling (p < 0.04) presented with late remodeling (increment of the end-diastolic volume > 20% at 6 months). In patients with early remodeling, the end-diastolic volume did not change significantly (101 +/- 13 vs. 94 +/- 22 ml/m2, NS) at 6 months; despite this, they maintained larger diastolic volumes than patients with late remodeling (81 +/- 12 ml/m2, p < 0.04) at 6 months. Infarction artery status did not influence the evolution of ventricular volumes and regional function. CONCLUSIONS: (1) A large infarct size is the main determinant of postinfarction remodeling. (2) Such infarct size-dependent ventricular dilation occurs early and does not tend to increase in late stage; in contrast, some cases of intermediate-large size infarcts without early remodeling exhibit late remodeling associated with a poor late recovery of regional function. (3) Recovery of regional function (indicating myocardial viability) rather than infarction artery status plays a role in the late ventricular remodeling process.

[Fetal cardiac arrhythmia characterized by Doppler echocardiography]. / Arritmia cardíaca fetal caracterizada mediante ecocardiografía-Doppler.

A fetal arrhythmia was detected in a pregnant woman. Fetal Doppler-echocardiography did not reveal cardiac structural alterations; the Doppler flow velocity recordings at the level of the left ventricular outflow tract revealed the continuous succession of three cardiac cycles: a prolonged cycle (456 +/- 6 ms, mean of five measurements), a medium duration cycle (428 +/- 4 ms) and a short cycle (296 +/- 4 ms) after which the prolonged cycle repeated. Identification of the late ventricle filling phase of the atrial systole in the Doppler flow velocity waveform during the long and medium duration cycles, the detection of the systolic movement of the atrial walls preceding contraction of the ventricle walls during the shortest cycle and the verification that summation of the shortest and longest cycles was inferior to twice the intervening cycle, supported the idea that the arrhythmia was produced by frequent atrial premature contractions (one every two sinus beats). The fetal arrhythmia progressively disappeared during pregnancy until delivery without complications, and the newborn's ECG only revealed sporadic premature atrial contractions.

[Extrinsic compression of the right atrium due to a mediastinal germ-cell tumor]. / Compresión extrínseca de la aurícula derecha por un tumor germinal mediastínico.

A patient with a mediastinal mass detected by plain chest roentgenogram is presented. The echocardiographic-Doppler examination and the computed tomography precise the gross nature and extent of the tumour and its anatomical location producing obstruction of the right atrium and modifying the blood flow pattern in this chamber. The serum tumour markers and the transthoracic biopsy confirm the diagnosis of primary mediastinal germ cell tumour.

[Induction of a double nodal pathway in dogs by transcatheter ablation with high frequency currents]. / Inducción de una doble vía nodal en el perro por ablación transcatéter con corrientes de alta frecuencia.

A dog weighing 15 kg and anesthetized with intravenous sodium thiopental was subjected to transcatheter ablation of the AV junction with high-frequency currents, in order to induce a partial alteration in AV conduction (first degree AV block). Two conventional bipolar electrode-catheters were introduced through the right femoral vein and used one for atrial pacing and the other for His bundle recording and current delivering. The catheter used for ablation was situated in the AV junction where the distal monopolar recording of the His bundle electrogram showed an A/V ratio close to one in the presence of His bundle deflection. Three discharges were delivered under continuous electrocardiographic monitoring. The output power used was 15 watts and current application time was up to five seconds after attaining complete AV block; 1:1 AV conduction was quickly restored on concluding discharge. After the second discharge, a discontinuous nodal function curve of the dual AV nodal pathway type was obtained (absent in control and after first discharge studies). Following the third discharge the conduction through the slow pathway was abolished. The study was repeated after four weeks, an a dual AV nodal pathway type curve similar to that found during the acute phase was obtained. The histologic findings showed a collagen scar partially replacing nodal tissue and creating a partial septation of the AV node. To conclude: The structural alterations of the AV node may induce a dual AV nodal pathway response.

[Hypertrophic myocardiopathy and ostium primum]. / Miocardiopatía hipertrófica y ostium primum.

A 45-year-old male with palpitations and a heart murmur was investigated. Echocardiography and haemodynamic study revealed the presence of a ostium primum type interatrial communication with left-right shunting and asymmetric hypertrophic heart disease. There was no subaortic obstruction, but anterior systolic movement of the mitral valve was detected that did not contact with the interventricular septum--in part due to the paradoxical motion of the latter. The possible benefit of surgery in this infrequent association is discussed, and a review is made of the literature.

[Transcatheter ablation with high-frequency currents as a method for creating useful experimental models in the study of cardiac conduction and automatism]. / Ablación transcatéter con corrientes de alta frecuencia como método para la creación de modelos experimentales útiles en el estudio de la conducción y el automatismo cardíacos.

PURPOSE: analyze the utility of transcatheter ablation with high-frequency currents to create different experimental models of altered cardiac automatism and conduction. METHOD: the results were obtained in six anesthetized dogs subjected to electrophysiological study after selectively applying transcatheter radiofrequency ablation to different zones of the specific cardiac conduction system. Ablation was carried out using conventional bipolar 7F catheter-electrodes. High-frequency currents (0.7 MHz) were emitted through the distal electrode, with variable intensity and duration according to the aim of the experiment. Anatomic (fluoroscopic) and electrophysiological criteria were used to position the electrode within the ablation zone. RESULTS: selective radiofrequency application to the atrioventricular junction zone affords complete A-V blocks with escape rhythms located in the A-V node or His-Purkinje system, together with different degrees of infra- and intra-hisian and intranodal blocks. The modification of intranodal refractoriness and conduction without interrupting atrial pulse transmission may manifest atypical patterns with truncated nodal conduction curves. The abolition of sinus function through ablation in the zone of the sulcus terminalis makes it possible to obtain supraventricular subsidiary rhythms. The obtaining of intranodal complete blocks with supra-Hisian escape rhythms demonstrates phenomena such as the modulation of subsidiary automatism by non-transmitted atrial pulses, analyzed by constructing phase-response curves. CONCLUSION: transcatheter ablation using high-frequency currents is useful in demonstrating phenomena related to intranodal and His-Purkinje conduction, subsidiary pacemaker automatism or the modulation of automatism and conduction via non-transmitted pulses.