PubMed Health⌕ Search

Biomedical subjects

Gustavo A Medrano

Publications and source records attributed to Gustavo A Medrano.

14 recordsLinked to original sources

Risk factors, echocardiographic patterns, and outcomes in patients with acute ventricular septal rupture during myocardial infarction.

Ventricular septal rupture (VSR), which can complicate an acute myocardial infarction (MI), carries a high mortality rate. Because precordial and transesophageal echocardiography can identify the type of rupture and assess right ventricular (RV) function at the patient's bedside, we examined the prognostic significance of echocardiographic patterns in postinfarct VSR by postulating that complex rupture and RV involvement carry a worse prognosis. Seventeen patients (10 men; mean age 66 years) who had confirmed postinfarct VSR underwent precordial and transesophageal echocardiography followed by coronary angiography. Serial 12-lead and right precordial leads were also available. Type of septal rupture was classified as simple or complex based on autopsy-proved echocardiographic criteria. Three patients had inferior wall MI and 14 had anterior wall MI. ST-segment elevation persisted >72 hours in all 3 patients who had inferior wall MI and in 12 who had anterior wall MI. Segmental wall motion abnormalities helped in detecting the left ventricular entry site, and use of unconventional views superimposed with color flow Doppler provided the RV exit site. RV function was better appreciated with transesophageal echocardiography. Two patients who had inferior wall MI and 7 who had anterior wall MI had complex ruptures. All 3 patients who had inferior wall MI and 7 who had anterior wall MI had electrocardiographic and echocardiographic evidence of RV involvement. Mortality rate was higher in patients who had complex rupture (78% vs 38%, p <0.001) and in those who had RV extension (71% vs 29%, p <0.001). In conclusion, persistent ST elevation is a common finding in patients who have postinfarct VSR. Complex VSR and RV involvement are significant determinants of clinical outcome.

Aged↗

[Early and late effects of adenosine in experimental ventricular tachycardia].

INTRODUCTION AND OBJECTIVE: To study the action of adenosine in experimental ventricular tachycardia. MATERIAL AND METHOD: We studied 173 mongrel dogs weighing 13-17 kg anesthetized with 30 mg/kg sodium pentobarbital given intravenously. Myocardial lesions were provoked with the injection of 1-1.5 mL phenol in the free wall of the left ventricle. Ventricular arrhythmia was induced 30 min later with aconitine crystals inserted into the periphery of the damaged area. The potential early and delayed antiarrhythmic action of adenosine was systematically investigated in 85 animals. Leads DII, aVR and aVL, unipolar right and left intraventricular leads, and one unipolar lead on the wall of the superior vena cava were used to record control tracings and tracings in the presence of myocardial damage during ventricular tachycardia and after injection of the drug. RESULTS: Sinus rhythm did not reappear in 72 control animals that did not receive adenosine. In the 63 animals with aconitine-induced ventricular tachycardia associated to myocardial damage, the optimal response to 6 mg adenosine-early and fleeting sinus rhythm-was seen in 45% of the dogs; delayed sinus rhythm was seen in 5%. In 67% of the 18 animals with ventricular tachycardia due only to myocardial damage, early and late sinus rhythm appeared with doses of 6 and 12 mg, and late sinus rhythm was seen with a dose of 12 mg. CONCLUSIONS: The antiarrhythmic action of adenosine was seen not only in ventricular tachycardia due to aconitine (triggered activity), but also in tachycardia induced by the myocardial damage (microreentries).

Adenosine↗

[ECG in ventricular hypertrophy].

The electrophysiological criteria for the diagnosis of ventricular hypertrophies, in the light of the sequence of ventricular depolarization and repolarization, are described. Hypertrophy of the right ventricle due to sustained systolic overloading can be global or segmental. In the first case, the magnitude and manifestation of the main vectors resulting from depolarization of this ventricle, i.e., IIs, IIr and IIIr, are increased. In the second case, the magnitude and manifestation of only some vectors resulting from its depolarization are increased; for example, vector IIr (right parietal) in the most frequent type of Fallot's tetralogy and vector IIIr (right basal) in chronic corpulmonale of obstructive origin. Left ventricular hypertrophy, which is generally of global type (aortic stenosis, systemic arterial hypertension), induces an increase in magnitude and manifestation of all the main vectors resulting from depolarization of this ventricle: I (first septal), II (left parietal) and III (left basal). But the left ventricular hypertrophy can also be of segmental type; for example, in idiopathic hypertrophic cardiomyopathy, in which the manifestation of an anteroseptal vector usually predominates. Biventricular hypertrophies produce different electrocardiographic patterns, depending on the preponderance of right or left electromotive ventricular forces. An example of electrocardiographic findings in biventricular hypertrophy is presented. It corresponds to an 18 year-old woman with a large patent ductus arteriosus compressing the left inferior laryngeal nerve, which produced a cardio-vocal syndrome. The patient had pulmonary and systemic hypertension and arterial hyposaturation. The surgical treatment of the patent ductus arteriosus normalized the pulmonary pressure as well as the arterial saturation.

Adolescent↗

[Non-complicated and complicated polyfascicular blocks].

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.

Bundle-Branch Block↗

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.

Animals↗

[On the clinical value of electrocardiogram].

Emphasis is given to the clinical value of the electrocardiogram, a simple, quick and unexpensive method for heart exploration. It provides functional information and reliably reflects the metabolic and electrolytic characteristics of myocardial fibers. Such an information cannot generally be obtained by other more sophisticated and expensive methods. The localization and extension of myocardial infarction, the positional and structural changes observed during the evolution of chronic cor pulmonale of obstructive origin, some characteristics of atrial and ventricular arrhythmias, the site of preexcitation in WPW syndrome and troubles due to a dysfunction of the ionic channels because of metabolic or genic alterations, are particularly examined. 1. A good correlation exists between the anatomical site and electrocardiographic indication of the infarcted area. 2. In the obstructive chronic cor pulmonale, positional and structural changes of the heart are observed. The first ones correspond to a vertical heart, due to a descent of the diaphragm and an increase of lung volume. The structural changes are due to an enlargement of the right heart: dilatation and hypertrophy. 3. Ventricular arrhythmias habitually present the "jumping wave" phenomenon between both septal masses and the consecutive aberrance of the ventricular complexes. 4. In the WPW syndrome, the thoracic circle permits to infer the site of preexcitation by the orientation of the first fronts of anomalous ventricular activation. 5. Modifications in the Q-Tc interval reflect the variations of ionic intracellular concentrations in a more reliable way than the changes of plasmatic concentrations. The aforementioned evidences the great usefulness of the electrocardiogram in the clinical setting.

Animals↗

[Electrical features of hypertrophied left heart].

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.

Heart Atria↗

[On metabolic therapeutics G-I-K in surgery of cardiac patients].

The basic principles of the metabolic therapeutics with glucose-insulin-potassium solutions, already proposed by Dr. Demetrio Sodi Pallares, are exposed. Chronologic succession of this treatment during the preoperative, transoperative and postoperative phases of heart surgery, as well as some personal observations of one of the authors, are described. The glucose-insulin-potassium solution is a powerful system, providing very useful energy to protect the injured myocardium during cardiovascular surgery. Many publications support this assertion. The most recent ones indicate a reduction of low output syndromes due to interventions on coronary arteries, as well as a significant diminution of circulating fatty acids after primary angioplasty. The mentioned solution, in higher concentrations than the initial one, could become routine therapeutics in medicine and surgery centers, in general.

Cardiac Surgical Procedures↗

[Septal and parietal dead myocardium with peripheral monofascicular blocks].

We describe the electrical manifestations of dead left septal, left and right parietal myocardium and those of biventricular location, reviewing the electrocardiographic signs of the isolated left and right peripheral blocks. We also describe the electrical manifestations of dead myocardium accompanied by a left anterior subdivision block (LASB) and a left posterior subdivision block (LPSB). These ventricular conduction disorders can reduce or conceal the electrical manifestation of the dead zone. We present a case in which a transient LASB conceals the electrical manifestation of dead anteroseptal myocardium. The association of diaphragmatic dead myocardium with LPSB reduces the electrocardiographic manifestation of dead tissue. We show the electrocardiographic findings obtained in a case of a biventricular anterior infarct with a right anterior subdivision block (RASB), as well as an ECG corresponding to the association of a dead myocardial zone with a right posterior subdivision block (RPSB). These ventricular conduction disorders do not generally conceal the electrocardiographic signs of dead myocardial tissue. The possible association of myocardial damage due to an infarct or a myocardiopathy with ventricular proximal and peripheral blocks must be kept in mind. Besides, it is important to consider that proximal blocks do not modify substantially the signs of dead myocardial tissue, whereas peripheral blocks can reduce or conceal these signs.

Bundle-Branch Block↗

[On Q-wave and non-Q wave myocardial infarcts].

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.

Electrocardiography↗

[Electrocardiographic features of right ventricular hypertrophy in chronic cor pulmonale].

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.

Adult↗

[On the ventricular arrhythmias in Chagasic chronic cardiomyopathy].

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.

Aged↗