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.

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.

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.

Modifications of mechanoelectric feedback induced by 2,3-butanedione monoxime and Blebbistatin in Langendorff-perfused rabbit hearts.

AIM: Myocardial stretching is an arrhythmogenic factor. Optical techniques and mechanical uncouplers are used to study the mechanoelectric feedback. The aim of this study is to determine whether the mechanical uncouplers 2,3-butanedione monoxime and Blebbistatin hinder or modify the electrophysiological effects of acute mechanical stretch. METHODS: The ventricular fibrillation (VF) modifications induced by acute mechanical stretch were studied in 27 Langendorff-perfused rabbit hearts using epicardial multiple electrodes and mapping techniques under control conditions (n = 9) and during the perfusion of 2,3-butanedione monoxime (15 mM) (n = 9) or Blebbistatin (10 µm) (n = 9). RESULTS: In the control series, myocardial stretch increased the complexity of the activation maps and the dominant frequency (DF) of VF from 13.1 ± 2.0 Hz to 19.1 ± 3.1 Hz (P < 0.001, 46% increment). At baseline, the activation maps showed less complexity in both the 2,3-butanedione monoxime and Blebbistatin series, and the DF was lower in the 2,3-butanedione monoxime series (11.4 ± 1.2 Hz; P < 0.05). The accelerating effect of mechanical stretch was abolished under 2,3-butanedione monoxime (maximum DF = 11.7 ± 2.4 Hz, 5% increment, ns vs baseline, P < 0.0001 vs. control series) and reduced under Blebbistatin (maximum DF = 12.9 ± 0.7 Hz, 8% increment, P < 0.01 vs. baseline, P < 0.0001 vs. control series). The variations in complexity of the activation maps under stretch were not significant in the 2,3-butanedione monoxime series and were significantly attenuated under Blebbistatin. CONCLUSION: The accelerating effect and increased complexity of myocardial activation during VF induced by acute mechanical stretch are abolished under the action of 2,3-butanedione monoxime and reduced under the action of Blebbistatin.

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.

Prognostic and therapeutic implications of dipyridamole stress cardiovascular magnetic resonance on the basis of the ischaemic cascade.

OBJECTIVE: To determine the prognostic and therapeutic implications of stress perfusion cardiovascular magnetic resonance (CMR) on the basis of the ischaemic cascade. SETTING: Single centre study in a teaching hospital in Spain. PATIENTS: Dipyridamole stress CMR was performed on 601 patients with ischaemic chest pain and known or suspected coronary artery disease. On the basis of the ischaemic cascade, patients were categorised in C1 (no evidence of ischaemia, n = 354), C2 (isolated perfusion deficit at stress first-pass perfusion imaging, n = 181) and C3 (simultaneous perfusion deficit and inducible wall motion abnormalities, n = 66). CMR-related revascularisation (n = 102, 17%) was defined as the procedure prompted by the CMR results and carried out within the next three months. RESULTS: During a median follow-up of 553 days, 69 major adverse cardiac events (MACE), including 21 cardiac deaths, 14 non-fatal myocardial infarctions and 34 admissions for unstable angina with documented abnormal angiography were detected. In non-revascularised patients (n = 499), the MACE rate was 4% (14/340) in C1, 20% (26/128) in C2 and 39% (12/31) in C3 (adjusted p value = 0.004 vs C2 and <0.001 vs C1). CMR-related revascularisation had neutral effects in C2 (20% vs 19%, 1.1 (0.5 to 2.4), p = 0.7) but independently reduced the risk of MACE in C3 (39% vs 11%, 0.2 (0.1 to 0.7), p = 0.01). CONCLUSIONS: Dypiridamole stress CMR is able to stratify risk on the basis of the ischaemic cascade. A small group of patients with severe ischaemia-simultaneous perfusion deficit and inducible wall motion abnormalities-are at the highest risk and benefit most from MACE reduction due to revascularisation.

Effects of chronic exercise on myocardial refractoriness: a study on isolated rabbit heart.

AIM: To determine whether chronic physical training increases atrial and ventricular refractoriness in isolated rabbit heart. METHODS: Trained rabbits were submitted to a protocol of treadmill running. The electrophysiological parameters of refractoriness investigated in an isolated heart preparation were: (1) atrial effective refractory period (AERP) and atrial functional refractory period and ventricular effective and functional refractory periods (VERP and VFRP) using the extrastimulus technique at four different pacing cycle lengths; (2) the dominant frequency (DF) of ventricular fibrillation (VF). A multi-electrode plaque containing 256 electrodes and a spectral method were used to obtain the mean, maximum and minimum DF of VF. Sinus cycle length of the isolated hearts was determined as an electrophysiological parameter of training. In vivo heart rate, myocardial heat shock proteins (HSP60) and inducible nitric oxide synthase were also determined in some animals as electrophysiological and biochemical markers of training respectively. RESULTS: VERP and VFRP were longer in the trained group than in the control group. The mean DF of VF was lower in the trained group than in the control group. Despite the fact that training did not significantly modify the AERP, it tended to be longer in the trained group (P = 0.09). CONCLUSION: Training seems to increase the electrical stability of ventricular myocardium. As the electrophysiological modifications were exhibited in hearts not submitted to extrinsic nervous system or humoral influences, they are, at least in part, intrinsic modifications. These electrophysiological data also suggest that training could protect against reentrant ventricular arrhythmias.

Microvascular perfusion 1 week and 6 months after myocardial infarction by first-pass perfusion cardiovascular magnetic resonance imaging.

OBJECTIVE: To characterise the evolution of myocardial perfusion during the first 6 months after myocardial infarction by first-pass perfusion cardiovascular magnetic resonance imaging (CMR) and determine its significance. DESIGN: Prospective cohort design. SETTING: Single-centre study in a teaching hospital in Spain. PATIENTS: 40 patients with a first ST-elevation myocardial infarction, single-vessel disease and thrombolysis in myocardial infarction (TIMI) grade 3 flow (stent in 33 patients) underwent rest and low-dose dobutamine CMR 7 (SD 1) and 184 (SD 11) days after infarction. Microvascular perfusion was assessed at rest by visual assessment and quantitative analysis of first-pass perfusion CMR. Of the 640 segments, 290 segments subtended by the infarct-related artery (IRA) were focused on. RESULTS: Both 1 week and 6 months after infarction, segments with normal perfusion showed more wall thickening, contractile reserve and wall thickness, and less transmural necrosis, p <0.05 in all cases. Of 76 hypoperfused segments at the first week, 47 (62%) normalised perfusion at the sixth month. However, 42 segments (14% of the whole group) showed chronic abnormal perfusion; these segments showed worse CMR indices in the late phase (p<0.05 in all cases). CONCLUSIONS: In patients with an open IRA, more than half of the segments with abnormal perfusion at the first week are normally perfused after six months. First-pass perfusion CMR shows that in a small percentage of segments, abnormal perfusion may become a chronic phenomenon-these areas have a more severe deterioration of systolic function, wall thickness, contractile reserve and the transmural extent of necrosis.

Risk stratification of patients with acute chest pain and normal troponin concentrations.

OBJECTIVE: To investigate the outcome of patients with acute chest pain and normal troponin concentrations. DESIGN: Prospective cohort design. SETTING: Single centre study in a teaching hospital in Spain. PATIENTS: 609 consecutive patients with chest pain evaluated in the emergency department by clinical history (risk factors and a chest pain score according to pain characteristics), ECG, and early (< 24 hours) exercise testing for low risk patients with physical capacity (n = 283, 46%). All had normal troponin concentrations after serial determination. MAIN OUTCOME MEASURES: Myocardial infarction or cardiac death during six months of follow up. RESULTS: 29 events were detected (4.8%). No patient with a negative early exercise test (n = 161) had events versus the 6.9% event rate in the remaining patients (p = 0.0001). Four independent predictors were found: chest pain score > or = 11 points (odds ratio (OR) 2.4, 95% confidence interval (CI) 1.1 to 5.5, p = 0.04), diabetes mellitus (OR 2.3, 95% CI 1.1 to 4.7, p = 0.03), previous coronary surgery (OR 3.1, 95% CI 1.3 to 7.6, p = 0.01), and ST segment depression (OR 2.8, 95% CI 1.3 to 6.3, p = 0.003). A risk score proved useful for patient stratification according to the presence of 0-1 (2.7% event rate), 2 (10.2%, p = 0.008), and 3-4 predictors (29.2%, p = 0.0001). CONCLUSIONS: A negative troponin result does not assure a good prognosis for patients coming to the emergency room with chest pain. Early exercise testing and clinical data should be carefully evaluated for risk stratification.

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.

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.

Mapping of atrial activation patterns after inducing contiguous radiofrequency lesions: an experimental study.

High resolution mapping techniques are used to analyze the changes in atrial activation patterns produced by contiguous RF induced lesions. In 12 Langendorff-perfused rabbit hearts, left atrial activation maps were obtained before and after RF induction of epicardial lesions following a triple-phase sequential protocol: (phase 1) three separate lesions positioned vertically in the central zone of the left atrial wall; (phase 2) the addition of two lesions located between the central lesion and the upper and lower lesions; and (phase 3) the placement of four additional lesions between those induced in the previous phases. In six additional experiments a pathological analysis of the individual RF lesions was performed. In phase 1 (lesion diameter = 2.8+/-0.2 mm, gap between lesions = 3+/-0.8 mm), the activation process bordered the lesions line in two (250-ms cycles) and four experiments (100-ms cycles). In phase 2, activation bordered the lesions line in eight (250-ms cycles, P < 0.01 vs control) and nine experiments (100-ms cycles, P < 0.001), and in phase 3 this occurred in all experiments except one (both cycles, P < 0.001 vs control). In the experiments with conduction block, the increment of the interval between activation times proximal and distal to the lesions showed a significant correlation to the length of the lesions (r = 0.68, P < 0.05, 100-ms cycle). In two (17%) experiments, sustained regular tachycardias were induced with reentrant activation patterns around the lesions line. In conclusion, in this acute model, atrial RF lesions with intact tissue gaps of 3 mm between them interrupt conduction occasionally, and conduction block may be frequency dependent. Lesion overlap is required to achieve complete conduction block lines. Tachycardias with reentrant activation patterns around a lesions line may be induced.

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.

[Epicardial mapping of reentrant activation during ventricular fibrillation. An experimental study]. / Cartografía epicárdica de la activación reentrante durante la fibrilación ventricular. Estudio experimental.

INTRODUCTION AND OBJECTIVES: High-resolution epicardial mapping was used in an experimental model to analyze reentrant activation during ventricular fibrillation. METHODS: In 30 isolated Langendorff-perfused rabbit hearts, recordings were made of ventricular fibrillation activity using an epicardial multiple electrode. In the activation maps with reentrant activation patterns, determinations were made of the number of consecutive rotations, the maximum length of the central core, the area encompassed by the core and two electrodes surrounding it, and the cycle defined by reentrant activation. RESULTS: Most of the activation maps analyzed showed complex patterns with two or more wave fronts that either collided or remained separated by functional block lines (514 maps, 86%). In 112 maps (19%) activation patterns compatible with epicardial breakthrough of the depolarization process were observed. Reentrant activity was recorded in 42 maps (7%) - the maximum number of consecutive rotations being 3 (mean = 1.3 +/- 0.5). The maximum length of the central core ranged from 3 to 7 mm (mean = 5 +/- 1 mm), while the area encompassed by the central core plus two electrodes surrounding it ranged from 35 to 55 mm2 (mean = 45 +/- 6 mm2). The reentrant cycle length (mean = 47 +/- 8 ms) showed a linear relation to the maximum length of the central core reentry (cycle = 4.52 x length + 24.6; r = 0.7; p < 0.0001). CONCLUSIONS: a) Epicardial mapping allowed the identification of reentrant activation patterns during ventricular fibrillation in the experimental model used; b) the reentrant activity detected is infrequent and unstable, and c) a linear relation exists between the duration of the cycles defined by reentrant activity and the maximum length of central core reentry.

[Determinants of contractile reserve in the infarction area. A quantitative study using dobutamine in contrast left ventriculography]. / Determinantes de la reserva contráctil en la zona del infarto. Estudio cuantitativo mediante ventriculografía de contraste con dobutamina.

AIM: The aim of this study was to relate the contractile reserve in infarction segments to the dysfunction at rest and to the residual coronary stenosis. METHODS: The study group consisted of 95 patients with a first myocardial infarction. Contrast left ventricular at baseline and after dobutamine infusion at 7.5 microg/kg/min and coronary angiograms were performed. The centerline method was used to quantify the extent of dysfunction (percentage of chords with dysfunction in the territory of the infarction artery) and its maximum severity (maximum units of standard deviation [SD] below the normal wall motion reference). Reduction of dysfunction extent with dobutamine was measured. RESULTS: On increasing baseline dysfunction severity, both the magnitude of the response to dobutamine ( 2 SD 3 SD 4 SD +/- 5 SD [n = 15] = 9+/-13%, > 5 SD [n = 13] = 3+/-4%, p = 0,0001), and the number of patients with a significant (> or =15%) positive response ( 2 SD 3 SD 4 SD 5 SD = 0%, p<0,0001) decreased. There were no differences in dobutamine improvement among the subgroups with (n = 84) or without (n = 11) significant stenosis in the infarction artery (18+/-15 vs. 16 +/-18%), or between the subgroups with a patent (n = 76, 18+/-19%) or occluded (n = 19, 11+/-11%) artery. CONCLUSIONS: Dobutamine response is related to dysfunction severity in the infarction area: when the severity is 5 (high negative response prevalence), dobutamine testing does not seem indicate. The existence of residual coronary stenosis does not attenuate contractile reserve at low dobutamine doses.