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[ES] La isquemia miocárdica aguda es un patología que causa aproximadamente 7 millones de muertes al año. Durante la primera fase de esta enfermedad cardiaca se producen potenciales de acción alternantes, que son fuertemente arritmogénicos. Sin embargo, aunque se dispone de estudios donde se han observado dichos alternantes experimentalmente, sus causas son aún desconocidas. El objetivo del presente TFG es doble. Por un lado, se ha partido de una versión del modelo de O'Hara-Rudy (O’Hara et al., 2011) de potencial de acción ventricular humano desarrollado por Ana González en su TFG (Gonzalez Ascaso, 2019) programado en Matlab y se ha desarrollado una versión que permite el estudio teórico de las causas de la aparición de potenciales de acción alternantes en situaciones de isquemia aguda de miocardio. El segundo objetivo consiste en determinar las causas de estos alternantes. Para ello, se ha programado un módulo nuevo para realizar de manera sistemática un elevado número de simulaciones que permiten identificar las condiciones que dan lugar a alternantes. Además, se han realizado distintas modificaciones de esta nueva versión del modelo para el estudio de los factores isquémicos y de las corrientes y concentraciones iónicas para tratar de dilucidar las causas de los mismos, y estudiar potenciales formas terapéuticas de eliminarlos. Los resultados obtenidos sugieren que los valores que toman las concentraciones intracelulares de ATP y ADP durante la isquemia aguda son clave en la aparición de alternantes eléctricos a través de la corriente de potasio sensible a ATP. También lo es la concentración extracelular de potasio. Por otro lado, la alternancia que se produce en el ciclo del calcio también tiene efectos en el potencial de acción, al provocar una alternancia en la corriente de calcio a través de los canales de tipo L. Asimismo, la depresión de la corriente rápida de sodio también ha probado ser clave en la aparición de alternantes. Por último, la corriente rápid, [EN] Acute myocardial ischemia is a disease that causes approximately 7 million deaths every year. During the first phase of this heart disease, alternans action potentials are produced, which are strongly arrhythmogenic. However, although there are studies where such alternans have been observed experimentally, their causes are still unknown. The aim of the present TFG is twofold. On the one hand, we have started from a version of the O’Hara-Rudy model (O’Hara et al., 2011) of the human ventricular action potential developed by Ana González during her TFG (Gonzalez Ascaso, 2019) programmed in Matlab and a version has been developed that allows the study, using computational models, of the causes of the appearance of alternans action potentials in situations of acute myocardial ischemia. The second objective is to determinate the causes of these alternans. A new module has then been programmed to systematically perform a large number of simulations to identify the conditions that lead to alternans. In addition, various modifications have been made to this new version of the model to study of ischemic factors and ionic currents and concentrations to try to elucidate the causes their causes and study potentials therapeutic ways of eliminating them. The results obtained suggest that the values taken by ATP, ADP and extracellular potassium during ischemia are key in the appearance of electrical alternants through the ATP-sensitive potassium current. On the other hand, the alternation that occurs in the calcium cycle also has effects on the action potentials, by causing an alternation in L-type calcium current. Likewise, depression of the fast sodium current has also been shown to be key in the occurrence of alternans. Finally, the fast potassium current favours the maintenance of these alternans action potentials, although it is not the direct cause of their appearance.

[ES] La isquemia miocárdica aguda es un patología que causa aproximadamente 7 millones de muertes al año. Durante la primera fase de esta enfermedad cardiaca se producen potenciales de acción alternantes, que son fuertemente arritmogénicos. Sin embargo, aunque se dispone de estudios donde se han observado dichos alternantes experimentalmente, sus causas son aún desconocidas. El objetivo del presente TFG es doble. Por un lado, se ha partido de una versión del modelo de O'Hara-Rudy (O’Hara et al., 2011) de potencial de acción ventricular humano desarrollado por Ana González en su TFG (Gonzalez Ascaso, 2019) programado en Matlab y se ha desarrollado una versión que permite el estudio teórico de las causas de la aparición de potenciales de acción alternantes en situaciones de isquemia aguda de miocardio. El segundo objetivo consiste en determinar las causas de estos alternantes. Para ello, se ha programado un módulo nuevo para realizar de manera sistemática un elevado número de simulaciones que permiten identificar las condiciones que dan lugar a alternantes. Además, se han realizado distintas modificaciones de esta nueva versión del modelo para el estudio de los factores isquémicos y de las corrientes y concentraciones iónicas para tratar de dilucidar las causas de los mismos, y estudiar potenciales formas terapéuticas de eliminarlos. Los resultados obtenidos sugieren que los valores que toman las concentraciones intracelulares de ATP y ADP durante la isquemia aguda son clave en la aparición de alternantes eléctricos a través de la corriente de potasio sensible a ATP. También lo es la concentración extracelular de potasio. Por otro lado, la alternancia que se produce en el ciclo del calcio también tiene efectos en el potencial de acción, al provocar una alternancia en la corriente de calcio a través de los canales de tipo L. Asimismo, la depresión de la corriente rápida de sodio también ha probado ser clave en la aparición de alternantes. Por último, la corriente rápid, [EN] Acute myocardial ischemia is a disease that causes approximately 7 million deaths every year. During the first phase of this heart disease, alternans action potentials are produced, which are strongly arrhythmogenic. However, although there are studies where such alternans have been observed experimentally, their causes are still unknown. The aim of the present TFG is twofold. On the one hand, we have started from a version of the O’Hara-Rudy model (O’Hara et al., 2011) of the human ventricular action potential developed by Ana González during her TFG (Gonzalez Ascaso, 2019) programmed in Matlab and a version has been developed that allows the study, using computational models, of the causes of the appearance of alternans action potentials in situations of acute myocardial ischemia. The second objective is to determinate the causes of these alternans. A new module has then been programmed to systematically perform a large number of simulations to identify the conditions that lead to alternans. In addition, various modifications have been made to this new version of the model to study of ischemic factors and ionic currents and concentrations to try to elucidate the causes their causes and study potentials therapeutic ways of eliminating them. The results obtained suggest that the values taken by ATP, ADP and extracellular potassium during ischemia are key in the appearance of electrical alternants through the ATP-sensitive potassium current. On the other hand, the alternation that occurs in the calcium cycle also has effects on the action potentials, by causing an alternation in L-type calcium current. Likewise, depression of the fast sodium current has also been shown to be key in the occurrence of alternans. Finally, the fast potassium current favours the maintenance of these alternans action potentials, although it is not the direct cause of their appearance.

[ES] La isquemia miocárdica aguda es un patología que causa aproximadamente 7 millones de muertes al año. Durante la primera fase de esta enfermedad cardiaca se producen potenciales de acción alternantes, que son fuertemente arritmogénicos. Sin embargo, aunque se dispone de estudios donde se han observado dichos alternantes experimentalmente, sus causas son aún desconocidas. El objetivo del presente TFG es doble. Por un lado, se ha partido de una versión del modelo de O'Hara-Rudy (O’Hara et al., 2011) de potencial de acción ventricular humano desarrollado por Ana González en su TFG (Gonzalez Ascaso, 2019) programado en Matlab y se ha desarrollado una versión que permite el estudio teórico de las causas de la aparición de potenciales de acción alternantes en situaciones de isquemia aguda de miocardio. El segundo objetivo consiste en determinar las causas de estos alternantes. Para ello, se ha programado un módulo nuevo para realizar de manera sistemática un elevado número de simulaciones que permiten identificar las condiciones que dan lugar a alternantes. Además, se han realizado distintas modificaciones de esta nueva versión del modelo para el estudio de los factores isquémicos y de las corrientes y concentraciones iónicas para tratar de dilucidar las causas de los mismos, y estudiar potenciales formas terapéuticas de eliminarlos. Los resultados obtenidos sugieren que los valores que toman las concentraciones intracelulares de ATP y ADP durante la isquemia aguda son clave en la aparición de alternantes eléctricos a través de la corriente de potasio sensible a ATP. También lo es la concentración extracelular de potasio. Por otro lado, la alternancia que se produce en el ciclo del calcio también tiene efectos en el potencial de acción, al provocar una alternancia en la corriente de calcio a través de los canales de tipo L. Asimismo, la depresión de la corriente rápida de sodio también ha probado ser clave en la aparición de alternantes. Por último, la corriente rápid, [EN] Acute myocardial ischemia is a disease that causes approximately 7 million deaths every year. During the first phase of this heart disease, alternans action potentials are produced, which are strongly arrhythmogenic. However, although there are studies where such alternans have been observed experimentally, their causes are still unknown. The aim of the present TFG is twofold. On the one hand, we have started from a version of the O’Hara-Rudy model (O’Hara et al., 2011) of the human ventricular action potential developed by Ana González during her TFG (Gonzalez Ascaso, 2019) programmed in Matlab and a version has been developed that allows the study, using computational models, of the causes of the appearance of alternans action potentials in situations of acute myocardial ischemia. The second objective is to determinate the causes of these alternans. A new module has then been programmed to systematically perform a large number of simulations to identify the conditions that lead to alternans. In addition, various modifications have been made to this new version of the model to study of ischemic factors and ionic currents and concentrations to try to elucidate the causes their causes and study potentials therapeutic ways of eliminating them. The results obtained suggest that the values taken by ATP, ADP and extracellular potassium during ischemia are key in the appearance of electrical alternants through the ATP-sensitive potassium current. On the other hand, the alternation that occurs in the calcium cycle also has effects on the action potentials, by causing an alternation in L-type calcium current. Likewise, depression of the fast sodium current has also been shown to be key in the occurrence of alternans. Finally, the fast potassium current favours the maintenance of these alternans action potentials, although it is not the direct cause of their appearance.

[ES] Una mejor comprensión de los mecanismos subyacentes a las arritmias ventriculares, así como una mejora de las terapias eléctricas y farmacológicas asociadas, son un factor clave para prevenir la muerte súbita cardíaca en pacientes con cardiopatías estructurales y eléctricas. Una miocardiopatía importante que puede provocar arritmias ventriculares potencialmente mortales es la insuficiencia cardíaca (HF). Los pacientes con HF a menudo sufren también de bloqueo de rama izquierda (LBBB) que deteriora su condición. Actualmente, el tratamiento más eficaz para estos pacientes es la terapia de resincronización cardíaca (CRT). Sin embargo, no se alcanza una respuesta positiva en todos los casos, por lo que es necesario un mayor estudio para mejorar este tratamiento. Una segunda patología cardíaca que también produce arritmias letales es la isquemia miocárdica. Evidencia experimental ha demostrado que las alteraciones electrofisiológicas en el miocardio ventricular constituyen un sustrato para la generación de arritmias durante la fase aguda de isquemia. Estas alteraciones son inducidas por los tres componentes isquémicos principales: hipercalemia, hipoxia y acidosis. Sin embargo, la influencia de cada componente en los mecanismos de inicio y mantenimiento de las arritmias no se comprende aún con claridad. Una primera parte de esta tesis doctoral, se centra en la optimización de la CRT durante su aplicación en un corazón que padece HF y LBBB. Para esto, se modificó el modelo de potencial de acción (AP) de O'Hara para simular una velocidad de conducción realista tanto en condiciones sanas como patológicas. Además, se estimó e incorporó un sistema de His-Purkinje (HPS) dentro de un modelo biventricular/torso humano 3D para simular un LBBB realista. A continuación, se desarrolló un conjunto de simulaciones computacionales para diferentes configuraciones de la CRT a fin de determinar la posición y el instante de estimulación óptimo que conducen a la duración más corta del Q, [EN] A better understanding of the mechanisms underlying ventricular arrhythmias, as well as an improvement of the associated electrical and pharmacological therapies, are a key factor to prevent sudden cardiac death in patients with structural and electrical heart diseases. An important cardiomyopathy that can lead to life-threatening ventricular arrhythmias is heart failure (HF). Patients with HF also often suffer from left bundle branch block (LBBB), which worsens their condition. Currently, the most effective treatment to these patients is cardiac resynchronization therapy (CRT). However, many patients are non-responders, so further studies are needed to improve this treatment. A second cardiac pathology that also produces lethal arrhythmias is myocardial ischemia. Substantial experimental evidence has shown that electrophysiological alterations in the ventricular myocardium constitute a substrate for the generation of arrhythmias during the acute phase of ischemia. These alterations are induced by the three main ischemic components: hyperkalemia, hypoxia and acidosis. However, the influence of each component in the mechanisms of arrhythmia initiation and maintenance is still not completely understood. In the first section of this doctoral thesis, we focus on the optimization of CRT during its application in a heart suffering from HF and LBBB. For this purpose, we modified the O'Hara action potential (AP) model to simulate a realistic conduction velocity both in healthy and pathological conditions. In addition, a His-Purkinje system (HPS) was generated and incorporated into a 3D human biventricular/torso model to simulate realistic LBBB. A set of computational simulations were performed for different CRT configurations to determine the optimal pacing leads location and delay values leading to the shortest QRS duration. Subsequently, results were compared with other optimization criteria. The main findings of this study showed the need of better or complementary, [CA] Una millor comprensió dels mecanismes subjacents a les arrítmies ventriculars, així com una millora de les teràpies elèctriques i farmacològiques associades, són un factor clau per a previndre la mort sobtada cardíaca en pacients amb cardiopaties estructurals i elèctriques. Una miocardiopatia important que pot provocar arrítmies ventriculars potencialment mortals és la insuficiència cardíaca (HF). Els pacients amb HF sovint pateixen també de bloqueig de branca esquerra (LBBB) que deteriora la seua condició. Actualment, el tractament més eficaç per a aquests pacients és la teràpia de resincronització cardíaca (CRT). No obstant això, no s'aconsegueix una resposta positiva en tots els casos, per la qual cosa és necessari un major estudi per a millorar aquest tractament. Una segona patologia cardíaca que també produeix arrítmies letals és la isquèmia miocàrdica. Evidència experimental ha demostrat que les alteracions electrofisiològiques en el miocardi ventricular constitueixen un substrat per a la generació d'arrítmies durant la fase aguda d'isquèmia. Aquestes alteracions són induïdes pels tres components isquèmics principals: hipercalèmia, hipòxia i acidosi. No obstant això, la influència de cada component en els mecanismes d'inici i manteniment de les arrítmies no es comprén encara amb claredat. Una primera part d'aquesta tesi doctoral, se centra en l'optimització de la CRT durant la seua aplicació en un cor que pateix HF i LBBB. Per a això, es va modificar el model de potencial d'acció (AP) de O'Hara per a simular una velocitat de conducció realista tant en condicions sanes com patològiques. A més, es va estimar i es va incorporar un sistema de His-Purkinje (HPS) dins d'un model biventricular/tors humà 3D per a simular un LBBB realista. A continuació, es va desenvolupar un conjunt de simulacions computacionals per a diferents configuracions de la CRT a fi de determinar la posició i l'instant d'estimulació òptim que condueixen a la duració més curta del QRS. Pos

[ES] La isquemia miocárdica aguda es un patología que causa aproximadamente 7 millones de muertes al año. Durante la primera fase de esta enfermedad cardiaca se producen potenciales de acción alternantes, que son fuertemente arritmogénicos. Sin embargo, aunque se dispone de estudios donde se han observado dichos alternantes experimentalmente, sus causas son aún desconocidas. El objetivo del presente TFG es doble. Por un lado, se ha partido de una versión del modelo de O'Hara-Rudy (O’Hara et al., 2011) de potencial de acción ventricular humano desarrollado por Ana González en su TFG (Gonzalez Ascaso, 2019) programado en Matlab y se ha desarrollado una versión que permite el estudio teórico de las causas de la aparición de potenciales de acción alternantes en situaciones de isquemia aguda de miocardio. El segundo objetivo consiste en determinar las causas de estos alternantes. Para ello, se ha programado un módulo nuevo para realizar de manera sistemática un elevado número de simulaciones que permiten identificar las condiciones que dan lugar a alternantes. Además, se han realizado distintas modificaciones de esta nueva versión del modelo para el estudio de los factores isquémicos y de las corrientes y concentraciones iónicas para tratar de dilucidar las causas de los mismos, y estudiar potenciales formas terapéuticas de eliminarlos. Los resultados obtenidos sugieren que los valores que toman las concentraciones intracelulares de ATP y ADP durante la isquemia aguda son clave en la aparición de alternantes eléctricos a través de la corriente de potasio sensible a ATP. También lo es la concentración extracelular de potasio. Por otro lado, la alternancia que se produce en el ciclo del calcio también tiene efectos en el potencial de acción, al provocar una alternancia en la corriente de calcio a través de los canales de tipo L. Asimismo, la depresión de la corriente rápida de sodio también ha probado ser clave en la aparición de alternantes. Por último, la corriente rápid, [EN] Acute myocardial ischemia is a disease that causes approximately 7 million deaths every year. During the first phase of this heart disease, alternans action potentials are produced, which are strongly arrhythmogenic. However, although there are studies where such alternans have been observed experimentally, their causes are still unknown. The aim of the present TFG is twofold. On the one hand, we have started from a version of the O’Hara-Rudy model (O’Hara et al., 2011) of the human ventricular action potential developed by Ana González during her TFG (Gonzalez Ascaso, 2019) programmed in Matlab and a version has been developed that allows the study, using computational models, of the causes of the appearance of alternans action potentials in situations of acute myocardial ischemia. The second objective is to determinate the causes of these alternans. A new module has then been programmed to systematically perform a large number of simulations to identify the conditions that lead to alternans. In addition, various modifications have been made to this new version of the model to study of ischemic factors and ionic currents and concentrations to try to elucidate the causes their causes and study potentials therapeutic ways of eliminating them. The results obtained suggest that the values taken by ATP, ADP and extracellular potassium during ischemia are key in the appearance of electrical alternants through the ATP-sensitive potassium current. On the other hand, the alternation that occurs in the calcium cycle also has effects on the action potentials, by causing an alternation in L-type calcium current. Likewise, depression of the fast sodium current has also been shown to be key in the occurrence of alternans. Finally, the fast potassium current favours the maintenance of these alternans action potentials, although it is not the direct cause of their appearance.

Electrophysiological alterations of the myocardium caused by acute ischemia constitute a pro-arrhythmic substrate for the generation of potentially lethal arrhythmias. Experimental evidence has shown that the main components of acute ischemia that induce these electrophysiological alterations are hyperkalemia, hypoxia (or anoxia in complete artery occlusion), and acidosis. However, the influence of each ischemic component on the likelihood of reentry is not completely established. Moreover, the role of the His-Purkinje system (HPS) in the initiation and maintenance of arrhythmias is not completely understood. In the present work, we investigate how the three components of ischemia affect the vulnerable window (VW) for reentry using computational simulations. In addition, we analyze the role of the HPS on arrhythmogenesis. A 3D biventricular/torso human model that includes a realistic geometry of the central and border ischemic zones with one of the most electrophysiologically detailed model of ischemia to date, as well as a realistic cardiac conduction system, were used to assess the VW for reentry. Four scenarios of ischemic severity corresponding to different minutes after coronary artery occlusion were simulated. Our results suggest that ischemic severity plays an important role in the generation of reentries. Indeed, this is the first 3D simulation study to show that ventricular arrhythmias could be generated under moderate ischemic conditions, but not in mild and severe ischemia. Moreover, our results show that anoxia is the ischemic component with the most significant effect on the width of the VW. Thus, a change in the level of anoxia from moderate to severe leads to a greater increment in the VW (40 ms), in comparison with the increment of 20 ms and 35 ms produced by the individual change in the level of hyperkalemia and acidosis, respectively. Finally, the HPS was a necessary element for the generation of approximately 17% of reentries obtained. The retrogr

The influence of each ischemic component (hypoxia, hyperkalemia, and acidosis) on arrhythmogenesis is controversial and difficult to study experimentally. In the present study, we investigate how the different ischemic components affect the vulnerable window (VW) for reentry using computational simulations. Simulations were performed in a 3D biventricular model that includes a realistic ischemic region and the His-Purkinje conduction system. At the cellular level, we used a modified version of the O’Hara action potential model adapted to simulate acute ischemia. Three different levels of ischemia were simulated: mild, moderate, and severe. The effects on the width of the VW of each ischemic parameter were analyzed. The model allowed us to obtain a realistic reentrant pattern corresponding to ventricular tachycardia in all simulations. Results suggest that the ischemic level plays an important role in the generation of reentries. Furthermore, hypoxia has the most significant effect on the width of the VW. The presence of Purkinje system is key to the generation of reentries.

This article presents modern literature sources on methods for determining acute myocardial ischemia. The diagnostic capabilities as well as the advantages and disadvantages when performing forensic medical examinations for cause of death have been highlighted., В статье представлены данные современных литературных источников о методах определения острой ишемии миокарда. Описаны их диагностические возможности, преимущества и недостатки при проведении судебно-медицинских экспертиз для диагностики причины наступления смерти., У статті представлені дані сучасних джерел літератури про методи визначення гострої ішемії міокарда. Описано їх діагностичні можливості, переваги та недоліки при проведенні судово-медичних експертиз для діагностики причини настання смерті.

Background In patients with symptoms compatible with acute myocardial infarction (MI), early triage by ECG in the pre-hospital phase by ST-segment elevation myocardial infarction (STEMI) criteria is important for direct transport of these patients to a regional center for primary percutaneous coronary intervention (pPCI). The time from first medical contact to pPCI should, due to present guidelines, be no longer than two hours. One main determinant of final infarct size (IS), in addition to myocardium at risk (MaR) and time to treatment, is the severity of ischemia, which relates to the rate of progression of the infarction wavefront. Presently, no assessment of severity is made. Patients with severe ischemia may have changes within the QRS complex in addition to ST-T changes, making it possible to identify these high-risk patients. QRS changes are, however more difficult to determine and to quantify correctly as compared to the changes within the ST segment. Aims and methods The overall objective was to increase the understanding of depolarization changes during myocardial ischemia and to evaluate whether these changes have possible clinical implications in patients with acute MI. Different QRS methods are applied in patients during ischemia produced by elective, prolonged PCI as well as during STEMI, and comparisons are made with conventional ECG parameters as well as single-photon emission computed tomography (SPECT) images. Results and conclusions Study I compared the computer-derived high-frequency QRS components (HF-QRS) in patients with and without standard ECG changes indicative of old MI. In contrast to previous findings we found that HF-QRS cannot differentiate between patients with and without old MI. Study II tested the ability of HF-QRS versus conventional ST-segment measurements to detect and quantify myocardial ischemia, as determined by SPECT, in a group of patients undergoing elective balloon PCI. We showed that HF-QRS can provide valuable informati

The accumulation of intermediates subsequent to impaired β-oxidation of free fatty acid (FFA) has been suggested as a cause of cellular damage in ischemic myocardium. ^<1-2> We investigated the effects of propranolol and diltiazem on carnitine metabolism in ischemic myocardium. Propranolol (0.2 mg/kg/min, i.v.) and diltiazem (0.1 mg/kg/min, i.v.) were administered for 5 min, the administration started 10 min before coronary occlusion. ECGs were continuously recorded throughout the experiment. Myocardial samples were prepared from both the non-ischemic and ischemic areas 40 min after coronary ligation. Adenosine triphosphate (ATP), free carnitine, long chain acyl carnitine and long chain acyl CoA were assayed. Propranolol reduced the decrease of ATP and the accumulation of long chain acyl CoA, induced by myocardial ischemia. Diltiazem reduced the decrease of ATP and free carnitine, and the accumulation of long chain acyl carnitine in the ischemic area. Propranolol and diltiazem significantly reduced the grade of ventricular arrhythmia. These results suggest that the protective mechanisms of propranolol and diltiazem on myocardium are based, at least in part, on their beneficial effects upon myocardial carnitine metabolism, rights:社団法人日本循環器学会, rights:本文データは学協会の許諾に基づきCiNiiから複製したものである

Background: Improved quantitative understanding of in vivo leaflet geometry in ischemic mitral regurgitation (IMR) is needed to improve reparative techniques, yet few data are available due to current imaging limitations. Using marker technology we tested the hypotheses that IMR (1) occurs chiefly during early systole; (2) affects primarily the valve region contiguous with the myocardial ischemic insult; and (3) results in systolic leaflet edge restriction. Methods: Eleven sheep had radiopaque markers sutured as five opposing pairs along the anterior (A1–E1) and posterior (A2–E2) mitral leaflet free edges from the anterior commissure (A1–A2) to the posterior commissure (E1–E2). Immediately postoperatively, biplane videofluoroscopy was used to obtain 4D marker coordinates before and during acute proximal left circumflex artery occlusion. Regional mitral orifice area (MOA) was calculated in the anterior (Ant-MOA), middle (Mid-MOA), and posterior (Post-MOA) mitral orifice segments during early systole (EarlyS), mid systole (MidS), and end systole (EndS). MOA was normalized to zero (minimum orifice opening) at baseline EndS. Tenting height was the distance of the midpoint of paired markers to the mitral annular plane at EndS. Results: Acute ischemia increased echocardiographic MR grade (0.5 ± 0.3 vs 2.3 ± 0.7, p < 0.01) and MOA in all regions at EarlyS, MidS, and EndS: Ant-MOA (7 ± 10 vs 22 ± 19 mm2, 1 ± 2 vs18 ± 16 mm2, 0 vs 17 ± 15 mm2); Mid-MOA (9 ± 13 vs 25 ± 17 mm2, 3 ± 6 vs 21 ± 19 mm2, 0 vs 25 ± 17 mm2); and Post-MOA (8 ± 10 vs 25 ± 16, 2 ± 4 vs 22 ± 13 mm2, 0 vs 23 ± 13 mm2), all p < 0.05. There was no change in MOA throughout systole (EarlyS vs MidS vs EndS) during baseline conditions or ischemia. Tenting height increased with ischemia near the central and the anterior commissure leaflet edges (B1–B2: 7.1 ± 1.8 mm vs 7.9 ± 1.7 mm, C1–C2: 6.9 ± 1.3 mm vs 8.0 ± 1.5 mm, both p < 0.05). Conclusions: MOA during ischemia was larger throughout systole, indica

Since the introduction of coronary angioplasty in 1977, this procedure has gained increasing importance in the treatment of coronary artery obstruction. From the available evidence it can be estimated that this therapeutic tool will gain even more momentum from the tens of thousands of patients who will be treated in the next few years. Information about the indications, benefits and risks of the coronary angioplasty is accumulating rapidly, in addition to publications about refinements of the technique itself. Recently, a number of investigators have realised that coronary angioplasty, is not only a therapeutic tool, but can, during the procedure. be used as a source of diagnostic information. When the catheter is placed across a coronary artery obstruction, inflation of the balloon produces transient myocardial ischemia. Before, during and after this period of severe ischemia studies of the performance of the myocardium at risk can be carried out. The fact that therapeutic coronary angioplasty is carried out in a cardiac catheterization laboratory, which is by definition optimally equipped for the measurements of hemodynamic parameters, has probably also contributed to the execution of these investigations. The combination of hemodynamic and biochemical parameters with morphological information from the coronary angiogram can be utilized for the quantification of myocardial involvement and the success of coronary artery dilatation with angioplasty. Studies of interactions with pharmacological substances are also feasible and informative. Coronary angioplasty has a most promising future as an unique means to gather insight in the intricacies of myocardial oxygen supply and demand in patients with coronary artery disease.