[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.

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

Un bloqueo de rama izquierda (BRIHH) de grado avanzado, i.e. con fenómeno de "salto de onda" extenso, hace que la activación septal anormal de origen a fuerzas electromotrices de mayor duración y magnitud respecto a las normales. Por eso se establece una preponderancia eléctrica septal respecto a las paredes libres ventriculares. La coexistencia de una zona de miocardio inactivable antero-septal con un BRIHH de grado avanzado hace que el "salto de onda" comience en porciones postero-septales inferiores. Por ende, los electrodos izquierdos externos ven alejarse los primeros frentes de la activación ventricular y registran ondas Q. La presencia de miocardio inactivable en la pared libre ventricular izquierda permite al electrodo externo correspondiente registrar la morfología del complejo intraventricular homolateral: R¯S. Un BRIHH de grado intermedio da origen a un "salto de onda" limitado de derecha a izquierda. Cuando dicho bloqueo se asocia a la presencia de miocardio inactivable septal, se reducen las manifestaciones del bloqueo izquierdo pero están presentes las de la necrosis: pérdida de la manifestación del primer vector septal derecho y registro de ondas Q en las derivaciones izquierdas. A causa de un bloqueo de rama derecha (BRDHH) de grado avanzado, con "salto de onda" extenso, también se originan fuerzas electromotrices septales predomi nantes. La coexistencia de una zona de miocardio inactivable anteroseptal con un BRDHH de grado avanzado hace que el "salto de onda" de izquierda a derecha comience en porciones postero-septales bajas. Así los electrodos de las derivaciones transicionales ven alejarse los primeros frentes del "salto de onda" y registran: ondas Q. Una zona inactivable parietal derecha, transmural, permite a los electrodos externos correspondientes registrar la morfología polifásica del complejo intra-ventricular homolateral. Un BRDHH de grado intermedio, asociado a necrosis antero-septal, se caracteriza por reducción de los signos de bloqueo y presencia de ondas Q en las derivaciones precordiales derechas y transicionales.

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: R¯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."

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

Se examinan algunos criterios acerca de los infartos definidos en la literatura actual como inferiores e inferolaterales. Con este fin, se describen los aspectos anatómicos del corazón aislado e in situ. Se analizan también las relaciones de este último con otros órganos torácicos circunvecinos. Se representa, de manera esquemática, el corazón como una pirámide con base triangular y sus lados y bordes en relación con las paredes de la caja torácica. Se resume, además, la orientación espacial de los principales vectores resultantes de los procesos de despolarización y repolarización ventriculares. Se subraya la utilidad del registro de las derivaciones unipolares torácicas posteriores V7, V8, V9 y del círculo torácico electrocardiográfico. Esto permite detectar la existencia de un infarto miocárdico agudo en regiones medias y básales de la pared inferolateral del corazón y su verdadera extensión. Con base en cotejos electroanatómicos previos, se concluye que las derivaciones V7 - V9 exploran los segmentos inferior e inferolateral en su tercio basal y medio, anteriormente denominados regiones cardiacas posterolaterales. Los registros electrocardiográficos proporcionan datos esencialmente funcionales y las imágenes obtenidas por resonancia magnética dan una información sobre todo estructural. Por lo tanto, ambos procedimientos de exploración cardiaca no deben contraponerse, sino integrarse.

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 electro-anatomical 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.

Bloqueos miocárdicos periféricos no complicados y complicados / Uncomplicated and complicated myocardial peripheral blocks

Septal necrosis + peripheral left blocks. Because of an extensive septal necrosis, the manifestation of the initial ventricular activation forces decreases in the precordial leads. With left bifascicular block (LASB + LPSB), the first ventricular activation forces become more evident and the electrical signs of septal necrosis can be 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 + left peripheral blocks. This 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. In turn, a coexisting trifascicular block causes the presence of QS complexes from V2 to V5. Posteroinferior necrosis + left peripheral blocks. Electromotive forces of the ventricular activation shift upward, due to a posteroinferior necrosis, and QS or QR complexes are recorded in leads aVF, II and III. An associated left bifascicular block displaces the main electromotive forces downward, posteriorly and to the left, due to a delay of the posteroinferior activation fronts. The ventricular complexes become positive and wider in all leads, reflecting the potential variations of the inferior portions of the left ventricle: aVF, II, III, sometimes V5 and V6. Consequently, the electrical signs of necrosis are reduced or abolished. Right ventricular peripheral blocks do not conceal the electrocardiographic signs of univentricular and biventricular dead myocardium.

Antiarrhythmic and arrhythmogenic action of inosine in experimental ventricular tachyarrhythmias.

OBJECTIVE: To study the possible action of inosine on experimental ventricular tachyarrhythmias. MATERIAL AND METHODS: We used 92 mongrel dogs weighing 13 kg-17 kg, anesthetized with 30 mg/kg sodium pentobarbital applied intravenously. Myocardial lesions were induced by injecting 1 ml-1.5 ml of 70% phenol in the free wall of the left ventricle. In 36 dogs, the ventricular arrhythmia (VT) was induced 30 min later with aconitine crystals inserted into the periphery of the damaged area; in 16, VT was due only to myocardial damage and in the other 13 VT was spontaneously originated. Twenty-nine animals constituted the control group; no inosine was administered to them. The possible effects of inosine were studied in 63 animals. Leads II, aVR or aVL, right and Left unipolar intraventricular leads and that on the wall of the superior vena cava were recorded under control conditions, once the myocardial damage had been induced, during the ventricular tachycardia, and following the injection of inosine. Of the 63 inosine-treated animals; in 34, VT was due to aconitine; in 16, it was produced only by the myocardial damage and, in 13, VT was presented spontaneously. RESULTS: Sinus rhythm was not reestablished in the animals of the control group. Inosine reestablished the sinus rhythm in 26 of 34 dogs (76%) that received phenol and aconitine, in 13 of the 16 (81%) presenting only the myocardial damage, and in 6 of the 13 (46%) with spontaneous ventricular tachycardia. In some experiments, inosine induced supraventricular tachycardias, ventricular-atrial blocks, and ventricular pre-excitation phenomena. CONCLUSIONS: In this experimental series, inosine showed antiarrhythmic and arrhythmogenic effects, similar to those of adenosine from which it derives.

[Uncomplicated and complicated myocardial peripheral blocks]. / Bloqueos miocárdicos periféricos no complicados y complicados.

Septal necrosis + peripheral left blocks. Because of an extensive septal necrosis, the manifestation of the initial ventricular activation forces decreases in the precordial leads. With left bifascicular block (LASB + LPSB), the first ventricular activation forces become more evident and the electrical signs of septal necrosis can be 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 + left peripheral blocks. This 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. In turn, a coexisting trifascicular block causes the presence of QS complexes from V2 to V5. Posteroinferior necrosis + left peripheral blocks. Electromotive forces of the ventricular activation shift upward, due to a posteroinferior necrosis, and QS or QR complexes are recorded in leads aVF, II and III. An associated left bifascicular block displaces the main electromotive forces downward, posteriorly and to the left, due to a delay of the posteroinferior activation fronts. The ventricular complexes become positive and wider in all leads, reflecting the potential variations of the inferior portions of the left ventricle: aVF, II, III, sometimes V5 and V6. Consequently, the electrical signs of necrosis are reduced or abolished. Right ventricular peripheral blocks do not conceal the electrocardiographic signs of univentricular and biventricular dead myocardium.

[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.

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

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.

Peripheral heart blocks associated with myocardial infarcts: clinical diagnosis based on experimental findings.

Septal necrosis + peripheral left blocks. Because of an extensive septal necrosis, the manifestation of the initial ventricular activation forces decreases in the precordial leads. With left bifascicular block (LASB + LPSB), the first ventricular activation forces become more evident and the electrical signs of septal necrosis can be concealed. In the presence of a trifascicular block, 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 V(1 )to V(4).Extensive anterior necrosis + peripheral blocks. This necrosis is manifested by QS complexes from V(2) to V(6). An associated left bifascicular block reduces the electrical manifestation of dead tissue: QS complexes persist only in V(3) and V(4). In turn, a coexisting trifascicular block causes the presence of QS complexes from V(2) to V(5). Posteroinferior necrosis + peripheral blocks. Electromotive forces of the ventricular activation shift upward, due to a posteroinferior necrosis and QS or QR complexes are recorded in leads aVF, II and III. An associated left bifascicular block displaces the main electromotive forces downward, posteriorly and to the left, due to a delay of the posteroinferior activation fronts. The ventricular complexes become positive and wider in all leads, reflecting the potential variations of the inferior portions of the left ventricle: aVF, II, III, sometimes V(5) and V(6). Consequently, the electrical signs of necrosis are reduced or abolished. Due to a trifascicular block, wide and slurred QS complexes are recorded in aVF, II, III and sometimes in V(5) and V(6).

[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.

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

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.

[Electrical manifestations of dead myocardium associated to proximal blocks of intermediate degree]. / Aspectos eléctricos de la asociación de miocardio inactivable y bloqueos tronculares de grado intermedio.

The electrical manifestation of dead myocardium associated to incomplete bundle branch block, i.e., with a limited "jumping wave" phenomenon, are exposed. Our description is based on previous experimental studies and validated by electro-anatomical comparisons. In previous experimental reports, the electrical manifestations of dead myocardium in the presence of varying degrees of associated block have also been described. The main electrocardiographic changes are related to the location and extent of damaged region and to degree of bundle branch block. If a left bundle branch block coexists with dead myocardium, small Q waves are registered in left unipolar leads exploring the damaged area. In these leads, the signs of subepicardial or transmural injury are increased. When a right proximal block coexists, the main changes concern the morphologies registered in the unipolar right epicardial and precordial leads. The electrical changes are due to the spatial orientation of the electromotive forces of ventricular depolarization and repolarization. The electrocardiographic changes described here can be satisfactorily understood in the light of the present knowledge on the ventricular electrical phenomenon.

Aspectos eléctricos de la asociación de miocardio inactivable y bloqueos tronculares de grado intermedio / Electrical manifestations of dead myocardium associated to proximal blocks of intermediate degree

The electrical manifestation of dead myocardium associated to incomplete bundle branch block, i.e., with a limited [quot ]jumping wave[quot ] phenomenon, are exposed. Our description is based on previous experimental studies and validated by electro-anatomical comparisons. In previous experimental reports, the electrical manifestations of dead myocardium in the presence of varying degrees of associated block have also been described. The main electrocardiographic changes are related to the location and extent of damaged region and to degree of bundle branch block. If a left bundle branch block coexists with dead myocardium, small Q waves are registered in left unipolar leads exploring the damaged area. In these leads, the signs of subepicardial or transmural injury are increased. When a right proximal block coexists, the main changes concern the morphologies registered in the unipolar right epicardial and precordial leads. The electrical changes are due to the spatial orientation of the electromotive forces of ventricular depolarization and repolarization. The electrocardiographic changes described here can be satisfactorily understood in the light of the present knowledge on the ventricular electrical phenomenon.

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

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 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.

En torno a las arritmias ventriculares en la miocardiopatía chagásica crónica / 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.

[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.

Aspectos electrocardiográficos de la hipertrofia ventricular derecha en el cor pulmonale crónico / 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.