Comparison of gastric reactance with commonly used perfusion markers in a swine hypovolemic shock model.

BACKGROUND: The gut has been hypothesized to be a protagonist tissue in multiple organ dysfunction syndrome (MODS) for the past three decades. Gastric reactance (XL) is a potential perfusion marker derived from gastric impedance spectroscopy (GIS), which is an emerging tool through which living tissue can be continuously measured to determine its pathophysiological evolution. This study aimed to compare the performance of XL [positive predictive values (PPV), negative predictive values (NPV), and area under the curve (AUC)] against commonly used perfusion markers before and during hypovolemic shock in swine subjects. METHODS: Prospective, controlled animal trial with two groups, control group (CG) N = 5 and shock (MAP ≤ 48 mmHg) group (SG) N = 16. Comparison time points were defined as T-2 (2 h before shock), T-1 (1 h before shock), T0 (shock), T1 (1 h after shock), and T2 (2 h after shock). Shock severity was assessed through blood gases, systemic and hemodynamic variables, and via histological examination for assessing inflammation-edema and detachment in the gastric mucosa. Macroscopic assessment of the gastric mucosa was defined in five levels (0-normal mucosa, 1-stippling or epithelial hemorrhage, 2-pale mucosa, 3-violet mucosa, and 4-marmoreal mucosa). Receiver Operating Characteristic (ROC) curves of perfusion markers and XL were calculated to identify optimal cutoff values and their individual ability to predict hypovolemic shock. RESULTS: Comparison among the CG and the SG showed statistically significant differences in XL measurements at T-1, T0, T1, and T2, while lactate showed statistically significant differences until T1 and T2. Statistically significant differences were detected in mucosa class (p < 0.001) and in inflammation-edema in the gastric body and the fundus (p = 0.021 and p = 0.043). The performance of the minimum XL value per subject  per event (XL_Min) was better (0.81 ≤ AUC ≤ 0.96, 0.93 ≤ PPV ≤ 1.00, 0.45 ≤ NPV ≤ 0.83) than maximum lactate value (Lac_Max) per subject per event (0.29 ≤ AUC ≤ 0.82, 0.82 ≤ PPV ≤ 0.91, 0.24 ≤ NPV ≤ 0.82). Cutoff values for XL_Min show progressive increases at each time point, while cutoff values for Lac_Max increase only at T2. CONCLUSIONS: XL proved to be an indirect and consistent marker of inadequate gastric mucosal perfusion, which shows significant and detectable changes before commonly used markers of global perfusion under the hypovolemic shock conditions outlined in this work.

Temperatus® software: A new tool to efficiently manage the massive information generated by iButtons.

An iButton is a temperature sensor of small dimensions (button-sized; 16 × 6 mm2), relatively low cost (˜US50$), with a stable and autonomous system that measures temperature and records the data in a protected memory section. These devices are used in different fields and the company offers a software (One-Wire Viewer) with several limitations. The present study describes Temperatus® software with the main aim of making the task of programming, downloading, and analysing the massive amount of data generated by iButtons smoothly, intuitive, time-efficient, and user-friendly.

[Left posterolateral extensive myocardial infarct. An electroanatomical comparison]. / Infarto posterolateral izquierdo extenso. Cotejo electro-anatómico.

A complete ECG thoracic circle allows exploring some heart structures not explored by the conventional electrocardiogram. It provides a direct indication on the location of the damaged myocardium. In fact, posterolateral infarctions can be limited to the inferior third of the left ventricle or can cover the entire free left ventricular wall from the base up to the heart apex and can be univentricular or biventricular. On the other side, the unipolar thoracic leads and the high abdominal leads MD, ME, MI show the evolution of the signs of injury, characteristic of the acute stage of infarction, toward necrosis. We present the example of a 61-year-old man, whose ECG shows signs of subepicardial or transmural injury and of necrosis in the low precordial leads V5 and V6, as well as in the high left posterior leads V8 and V9. This fact suggests the presence of an acute extensive myocardial infarction extending from the base to the heart apex. Moreover, the moderate elevation of the RS-T segment from to V9R to V7R indicates the presence of subepicardial injury in the high posterior regions of the right ventricular wall. These electrocardiographic data were confirmed by the radioactive isotope study and, definitively, by the anatomical findings.

[On the diagnostic value of indirect electrocadiographic signs of left posterolateral basal infarction]. / Acerca del valor diagnóstico de los hallazgos ECG indirectos de infarto miocárdico posterolateral basal izquierdo.

The left basal posterolateral infarct does not give pathological Q waves nor ventricular QS complexes in the low lateral leads V5 and V6. For that, the increased voltage of R waves in the lead V2 and or transitional leads V3 and V4, constitutes only an indirect sign of the presence of dead myocardium in the left posterolateral basal regions. Naturally, in these cases, a differential diagnosis with left ventricular or biventricular hypertrophy is mandatory. Therefore it is suitable to register left posterior thoracic leads V7-V9 or, preferably, a complete thoracic circle. We present here three examples: two experimental and another clinical, in which the electrocardiographic findings corresponded to anatomical data of a left posterolateral basal infarction. This fact speaks for a no absolute but relative diagnostic value of the indirect electrocardiographic signs of altered ventricular depolarization and repolarization in the left posterolateral basal regions of the left ventricle.

Pulmonary embolism as a cause of death in patients with heart disease: an autopsy study.

STUDY OBJECTIVE: To establish the prevalence of pulmonary embolism (PE) in autopsy material at a tertiary cardiac referral center and its importance as a cause of death in patients with heart disease (HD). DESIGN: Case series. SETTING: National Heart Institute, Mexico City. PATIENTS: One thousand thirty-two patients who died at our institution from 1985 to 1994 in whom an autopsy study was performed. MEASUREMENTS AND RESULTS: Of the 1,032 autopsies reviewed, 231 cases (24.4%) of PE were found; 100 of these patients had a diagnosis of massive PE. Massive PE (obstruction of either of the main pulmonary arteries or more than two lobar arteries) was found to be the third cause of death in this HD population. By age-group distribution, the global prevalence of massive events was higher in patients < 10 years old. Clinical suspicion (premortem) was raised in only 18% of the cases. CONCLUSIONS: PE was a frequent cause of morbidity and mortality in patients with HD who underwent autopsies. The incidence of massive PE was high in children.

[Electrocardiographic features of right ventricular hypertrophy in chronic cor pulmonale]. / Aspectos electrocardiográficos de la hipertrofia ventricular derecha en el cor pulmonale crónico.

The electrophysiological criteria for diagnosing right ventricular hypertrophy, characteristic of chronic cor pulmonale, are described. Right ventricular hypertrophy due to a sustained systolic overload can be global or regional. In the first situation, as for example, an idiopathic pulmonary hypertension, the magnitude and manifestation of all the main vectors resulting from the depolarization of this ventricle are increased: Ils (septal), llr (parietal), and Illr (basal). When the right ventricular hypertrophy is of the segmental (regional) type, as for example, that due to a chronic bronchial obstruction, the magnitude and manifestation of only some right vectors are increased. In this condition, only the magnitude of the right basal vector (Illr) is augmented. In the presence of subepicardial or transmural ischemia of the right ventricle, negative T waves of primary type are recorded in right precordial and transitional leads, where the Q-Tc interval is prolonged in the absence of digitalis effect. Two demonstrative examples of the correlations existing between the electrocardiographic and anatomical findings in global and regional hypertrophies, respectively, of the right ventricle are presented.

[On the ventricular arrhythmias in Chagasic chronic cardiomyopathy]. / En torno a las arritmias ventriculares en la miocardiopatía chagásica crónica.

Some authors have shown a high prevalence of electric circuits localized in the epicardium in Chagasic cardiomyopathy. Other authors have found in these patients, during electric mapping, mid-diastolic potentials and earlier myocardial activation in epicardial regions than in the endocardium. In a previous study, we found electrocardiographic signs of subepicardial ischemia in 66% of seropositive Chagasic patients against 16% of seronegative Chagasic ones. In the case presented here, a Chagasic dilated cardiomyopathy, we found electrocardiographic signs of subepicardial injury in the left free ventricular wall, related with histological findings of lymphocytic inflammation in these regions. In contrast, the endocardium was completely free from inflammation foci.

[An ECG-anatomical comparison in a case of Williams' syndrome]. / Cotejo electro-anatómico en un caso de síndrome de Williams.

A case of Williams' syndrome in a 22 years old man, is described. Clinical data, as well as those of laboratory and of imageneology study, are reported. An electro-anatomical comparison permitted to verify the value of electrocardiographic signs of enlargement of the four heart chambers, due to a mixed overload. It permitted also to establish the value of the signs of the interatrial block, probably due to myocardial atrial fibrosis, and those suggesting hyperkalemia. The electrocardiogram always is very useful because it furnishes certain functional aspects permitting to allow structural inferences, in following subjects with congenital or acquired heart diseases.

[On Q-wave and non-Q wave myocardial infarcts]. / Infartos miocárdicos con onda Q y sin onda Q.

Much has been said, and is still being said, on Q-wave and non-Q wave myocardial infarcts, trying to relate this electrocardiographic behavior with the culprit coronary arteries and the location of the damaged myocardium. However, it seems logic to bear in mind that the presence or absence of abnormal Q waves depends on the relation established between the zone of damaged myocardium and the width of the electrical endocardium. It must be recalled that the presence of normal Q waves is possible in leads that seem to move away from the first vector of ventricular activation. Besides, the electrical endocardium, i.e., the territory of distribution of Purkinje's network, is situated mainly in the lower half of the ventricles and is virtually absent in basal regions. This endocardium constitutes a histological-functional entity, since the Purkinje fibers, which receive at the same time the activation impulses, are depolarized simultaneously without producing differences in potential. Therefore, these fibers cannot supply an electrical contribution either in normal condition or in the presence of limited damage. Nevertheless, when the damaged zone reaches beyond the exterior limits of this endocardium, for example, in regions where it is small, the exploring electrode can register abnormal Q waves, due to the activation fronts that are moving away, followed by R waves originated in contiguous bands of non-damaged myocardium. We present two characteristic examples of the electrocardiographic manifestations of a transmural left ventricle infarct (QS complexes) and of a subendocardial infarct, reaching beyond the borders of the electrical endocardium (QR complexes). In both of these cases, the electrocardiographic data agree with the anatomical findings.

[Severe right ventricular hypertension secondary to metastatic obstruction due to hepatocarcinoma]. / Hipertensión ventricular derecha severa secundaria a obstrucción metastásica por hepatocarcinoma.

Right ventricular hypertension (RVH) is an entity that could be expected in various cardiopulmonary diseases. Mechanical obstruction to the right ventricle outflow tract is a cause of RVH. We present the case of a 69 year-old male with a history of hepatocarcinoma previously treated. The developed RVH due to mechanical obstruction secondary to metastatic infiltration of the right ventricle. The clinical syndrome was characterized by systemic venous hypertension. Non-invasive studies, such as electrocardiogram and computed tomography scan limited the metastasis to the right ventricle; the diagnosis was confirmed by cardio-angiography and endocardial biopsy. The studies did not demonstrate neoplastic activity at any other level.

[Electrical features of hypertrophied left heart]. / Aspectos eléctricos de la hipertrofia del corazón izquierdo.

Chronological and spatial characteristics of the main resultant vectors of the left atrial and ventricular depolarization in normal conditions and in presence of hypertrophy, due to a sustained overload, are described. The coexistence of interatrial, intraatrial, and intraventricular conduction disorders can modify the orientation of these vectors. The main electrocardiographic sign of left atrial hypertrophy is a P wave duration > 0.10 sec in adults. In case of left ventricle hypertrophy, the time of onset of the intrinsicoid deflection (TOID) is prolonged in the near left unipolar leads, and the S wave voltage is increased in opposite regions, i.e. in the right precordial or transitional leads. It is necessary to bear in mind other useful electrocardiographic signs. Hence, absence of the right basal vector (IIId) manifestation in a clockwise rotating heart is probably due to an increase in the basal electromotive forces of the left ventricle (vector IIIi) due to hypertrophy or ipsilateral ventricular conduction disorders. For a correct evaluation of these signs, it is mandatory to perform a rational analysis of the traings, not just a stereotyped electrical exploration. Besides it is very important to determine the Q-Tc interval in the left unipolar leads to establish whether, in these leads, the inverted T wave is of secondary type (normal Q-Tc) or of primary type (prolonged Q-Tc) due to a coexisting subepicardial or transmural ischemia. From these considerations, the usefulness of the thoracic circle and high abdominal unipolar leads is inferred.

[Non-complicated and complicated polyfascicular blocks]. / En torno a los bloqueos polifasciculares no complicados y complicados.

Septal necrosis + Peripheral blocks. Because of an extensive septal necrosis, the manifestation of the initial ventricular activation forces decreases in the precordial leads. With left bifascicular block, first ventricular activation forces become evident, and the electrical signs of a sepatal necrosis are concealed. In the presence of a trifascicular block, the manifestation of the first ventricular electromotive forces diminishes again and the electrical signs of septal necrosis become evident once more. Small Q waves are present in leads V1 to V4. Extensive anterior necrosis + Peripheral blocks. Such a necrosis is manifested by QS complexes from V2 to V6. An associated left bifascicular block reduces the electrical manifestation of dead tissue: QS complexes persist only in V3 and V4. A trifascicular block determines the presence of QS complexes from V2 to V5. Posteroinferior necrosis + Peripheral blocks. Electromotive forces of the ventricular activation shift upward, due to a posteroinferior necrosis. QS or QR complexes are recorded in leads a VF, II, and III. A left bifascicular block displaces the main electromotive forces downward, posteriorly and to the left, due to a delay of the posteroinferior activation. QRS complexes become positive and wider in all leads, the reflect the potential variations of the inferior portions of the left ventricle: aVF, II, and III, sometimes V5 and V6. The electrical signs of necrosis are reduced or abolished. With a trifascicular block, wide and slurred QS complexes appear in aVF, II, III, and sometimes in V5 and V6 too.

An experimental contribution to the concept of "jumping wave" phenomenon in the interventricular septum.

OBJECTIVE: The purpose of this study was to evaluate the existence of a histologically bipartite interventricular septum and the electrical independence of both septal masses, as well as to understand the changes of septal activation fronts in the presence of bundle branch blocks. METHODOLOGY: We examined the histological characteristics of both septal masses in 12 canine hearts. Furthermore, in another 11 anesthetized dog hearts, we analyzed morphological and chronological data of intraseptal records with normal activation and in the presence of proximal blocks. RESULTS: A histological discontinuity between the two septal masses in canine hearts seems to exist. Analysis of intraseptal and intracavitary electrical records confirmed slow transmission of the activation fronts from one septal mass to the other when proximal blocks were present. Morphological and chronological changes of the intracavitary complexes agree with the "jumping wave" phenomenon theory. CONCLUSIONS: These results support the validity of this approach to the activation of both septal masses and explain the chronological and morphological changes of the intracavitary records in the presence of ventricular blocks. In addition, this approach is a useful tool to detect the possible coexistence of dead septal tissue.

Cross-sex hormonal replacement: is this really effective? an experimental clue.

Castrated rats of either sex were used in this work, and sex hormones of their own gender or cross-sex hormones were administered for 4 months. Animals were then put through 5 min of myocardial ischemia followed by a 5-min reperfusion injury. Electrocardiographic recordings were made and serum was obtained. Sex hormone levels were measured. Cardiac frequency was calculated, arterial pressure was determined, and the levels of lactate dehydrogenase (LDH), creatinine kinase (CK), and thiobarbituric acid reactive species (TBARs) were analyzed. Proinflammatory cytokine levels were measured in homogenized hearts; besides this, five hearts of each experimental group were obtained and fixed for histopathologic analysis. In male rats with estradiol replacement, the incidence of tachyarrhythmias and CK levels were higher when compared to the rest of the animals. Their cytokine levels were also elevated when compared to the group that received testosterone. Estradiol replacement protected female rats from variations in all of the parameters evaluated, whereas testosterone did not show a protective effect. In the presence of testosterone, the incidence of tachyarrhythmia was higher and TBARs, cytokines, CK, and LDH levels were also elevated. The results shown reinforce the idea that cross-sex hormone administration can damage the cardiovascular system.

Sexual hormones: effects on cardiac and mitochondrial activity after ischemia-reperfusion in adult rats. Gender difference.

In this work we studied the influence of sex hormones on heart and mitochondrial functions, from adult castrated female and male, and intact rats. Castration was performed at their third week of life and on the fourth month animals were subjected to heart ischemia and reperfusion. Electrocardiogram and blood pressure recordings were made, cytokines levels were measured, histopathological studies were performed and thiobarbituric acid reactive species were determined. At the mitochondrial level respiratory control, transmembranal potential and calcium management were determined; Western blot of some mitochondrial components was also performed. Alterations in cardiac function were worst in intact males and castrated females as compared with those found in intact females and castrated males, cytokine levels were modulated also by hormonal status. Regarding mitochondria, in those obtained from hearts from castrated females without ischemia-reperfusion, all evaluated parameters were similar to those observed in mitochondria after ischemia-reperfusion. The results show hormonal influences on the heart at functional and mitochondrial levels.

[Ventricular conduction disorder in presence of dead myocardium]. / Trastornos de conducción ventricular y miocardio inactivable.

In the presence of an advanced degree left bundle branch block (LBBB) with an extensive "Jumping wave" phenomenon, the septal activation abnormally spreading originates septal electromotive forces of greater duration and consequently more important than normal ones. The coexistence of an inactive anteroseptal myocardium with an advanced degree block causes the phenomenon of "Jumping wave" begins in postero-septal regions. Therefore the external left electrodes see the first ventricular activation fronts moving away and register Q waves. The presence of transmural inactive myocardium in the free left ventricular wall permits the corresponding external electrodes to record the morphology of the ipsilateral intraventricular complex: S. An intermediate degree LBBB produces a limited right to left "Jumping wave" phenomenon. When it is associated to septal inactive myocardium, the electrical manifestations of left block are reduced, but those of myocardial necrosis persist: loss of the manifestation of first right septal vector and presence of Q waves in left leads. Because of an advanced degree right bundle branch block (RBBB) with an extensive "Jumping wave" phenomenon, electromotive septal forces of greater duration and consequently more important than normal ones, are originated also. The coexistence of inactive antero-septal myocardium with an advanced degree RBBB causes the phenomenon of "Jumping wave" begins in inferior postero-septal regions. Therefore, the transitional leads see the first fronts of the said phenomenon moving away and register Q waves. The presence of inactive transmural right parietal myocardium permits the corresponding external electrodes to record the morphology of the ipsilateral polyphasic intraventricular complex. An intermediate degree RBBB, associated to antero-septal necrosis, is characterized by the reduction of the electrocardiographic signs of the said block and the presence of Q waves in the right precordial and transitional leads.

[On the actual nomenclature of myocardial infarcts]. / Acerca de la denominación actual de infartos miocárdicos.

Certain criteria are examined for infarctions currents defined as inferior or inferolateral. To do this, certain considerations on the anatomical aspects of isolated and in situ heart are laid out. The topographical relationship of the in situ heart with other adjacent thoracic organs is described. The heart is schematically represented as a pyramid with a triangular base and its walls and borders are related to walls of the thorax. The spatial orientation of the main resulting vectors from ventricular depolarization and repolarization are summarized also. Usefulness of registering the unipolar thoracic leads V7, V8, V9 or a complete electrocardiographic thoracic circle, is underlined. This method allows to detect for of the existence of an acute myocardial infarction in the inferior and inferolateral segments in as third basal and mid cardiac regions previously denominated posterolateral. On the base of previous electroanatomical comparisons, it is concluded that the thoracic posterior leads V7 - V9, as well as the magnetic resonance images, explore the same heart regions. Therefore, these two methods: electrocardiography which is an essentially functional method and magnetic resonance that especially focus on structural changes are not contradictory but rather complementary tests."

In vivo assessment of hemocompatibility of a ventricular assist device in healthy swine.

OBJECTIVE: To assess the hemocompatible performance of a novel implantable pneumatic ventricular assist device (VAD, Innovamédica, México) in healthy swine. The aim of this pilot study was first, to determine if short-term VAD implantation elicited remarkable inflammatory response above that expected from surgical trauma; and second, to assess if heparinized or passivated VAD coatings, in combination with systemic anticoagulant or antiaggregant therapies, modified the VAD's hemocompatible performance. METHODS: Hemodynamic, physicologic, inflammatory and histological parameters were measured in 27 pigs receiving VAD support for six hours, testing combinations of heparinized or passivated VAD coatings and systemic anticoagulant/ antiaggregant therapies. Mean concentrations of interleukin -1 B (IL-1B), interleukin -6 (IL-6), C-reactive protein (CRP), or thrombin-antithrombin III (TAT) complexes (coagulation indicator) were measured from blood. ANOVA statistics were employed. RESULTS: No substantial increases in mean IL -1B, IL-6, CRP, or TAT were obtained during VAD support. Hemodynamic ans physiologic parameters were normal. We found no evidence of thromboembolisms or micro-infarctions in heart and lung samples. No major coaguli/deposits were found in VAD compartments. Overall, no remarkable differences in measurements were found using heparinized, passivated, or uncoated VAD, or with systemic anticoagulation, antiaggregant therapy, or no treatment. CONCLUSIONS: Our findings demonstrate, firstly, that during the time-period tested, the VAD elicited negligible inflammation above the effects of surgical trauma; and secondly, that little coagulation was observed upon VAD support in any of the cases tested. Contemplating further validation studies, our data indicate that the Innovamédica VAD is a highly hemocompatible system.