The role of pulmonary pressure/cardiac index to identify pulmonary hemodynamic responders to acute oxygen breathing pulmonary hypertension COPD patients / La utilidad de la relación presión arterial pulmonar - índice cardiaco para identificar respondedores hemodinámicos a la administración aguda de oxígeno en sujetos con enfermedad pulmonar obstructiva crónica e hipertensión pulmonar

Objectives: We sought to analyze exercise-derived mean pulmonary artery pressure (Mpap) - cardiac index (CI) - relationship to expand the concepts regarding its nature and to better identify pulmonary hemodynamic responders to acute oxygen breathing (AOB - 99.5%) in pulmonary hypertension (PH) - COPD patients. Methods: mPAP/CI and extrapolated pressure (Pext) to zero flow were obtained breathing room air (BRA) and under AOB - 99.5% in 40 stable COPD patients with rest and exercise PH. Hemodynamic characteristics were analyzed for the entire cohort and separate for cases those with resting < or > 30 mmHg mPAP (cohort - A and B, respectively). Results: mPAP/CI abnormal location, slope (Sp: 5.77; 95% CI: 5.02 - 6.52 mmHg/L min/m²) and Pext values (15.8 mmHg) were associated with hypoxemia/decreased mixed venous - PO2 and lung mechanics abnormalities. Hemodynamic conditions that did not change for Sp (5.47; 95% CI: 3.64 - 7.3 mmHg/L min/m², p = 0.4) and Pext (15.7 mmHg, p = 0.2) associated with a mPAP/CI significantly decrease in parallel during AOB - 99.5%. For cohort - A, an average-mPAP decline (12.3 mmHg, p <0.004) associated with a slope decrease (from 6.02; 95% CI: 4.04 - 8 to 4.3; 95% CI: 4.11 - 4.49 mmHg/L min/m², (p <0.008), mPAP/CI - 95% CI down-ward displacement and Pext decrease (from 8.58 ± 3 to 4.7 ± 1.4 mmHg, p <0.01) in relation to BRA were observed. For cohort-B, average-mPAP and mPAP/CI - 95% CI location did not change, Sp show a trend to decrease (p = 0.08) and Pext significantly increase (from 12 ± 2.9 to 20.6 ± 4.9 mmHg, p <0.03) in relation to BRA. Under AOB - 99.5%, significant differences for mPAP/ CI - 95% CI location, average-mPAP (A: 19.5 ± 6 vs. B: 41.2 ± 11.5 mmHg, p <0.001) and Pext (A: 4.7 ± 1.4 vs. B: 20.6 ± 4.9 mmHg, p <0.001), without Sp change between cohorts A and B were documented. Conclusions: When exercise derived mPAP/CI is analyzed, valuable information for linear-pulmonary vascular resistance - (LPVR) could be obtained for PH - COPD patients. mPAP/CI abnormalities not always reflect "pure arteriolar" increased LPVR for all PH-COPD patients. Hemodynamic benefit on the pulmonary circulation and right ventricular afterload could be expected with long-term oxygen therapy in resting <30 mmHg mPAP-PH-COPD patients.

Objetivos: En esta investigación clínica-hemodinámica, analizamos la relación que se establece entre la presión arterial pulmonar media (PAPm) con la del índice cardiaco (IC), obtenida durante el ejercicio, con miras a expandir los conceptos relacionados con su propia naturaleza. Con ello, tratar de identificar mejor a los sujetos portadores de EPOC que se han caracterizado por ser respondedores durante la administración aguda de oxígeno (AAO2 - 99.5%). Métodos: Se obtuvieron la PAPm/IC y la presión extrapolada a cero flujo (Pext = bo)en 40 sujetos con EPOC y portadores de hipertensión pulmonar (HP) clínicamente estables, respirando aire ambiental (RAA) y bajo la influencia de la AAO2 - 99.5% en las condiciones de reposo y durante el ejercicio. Las características hemodinámicas se analizaron para toda la cohorte y para aquellos sujetos con PAPm en resposo < o > de 30 mmHg (Cohorte A y B, respectivamente). Resultados: La ubicación anormal de la PAPm/IC, de la pendiente (Sp: 5.77; 95% IC: 5.02 - 6.52 mmHg/L min/m²) y la de los valores para Pext (15.8 mmHg) se asociaron con: hipoxemia/ disminución de la presión venosa mezclada del O2, así como con anormalidades de la mecánica pulmonar. Condiciones hemodinámicas que no se modificaron para la Sp (5.47; 95% IC: 3.64 - 7.3 mmHg/L min/m², p = 0.4) y la Pext (15.7 mmHg, p = 0.2); sin embargo, sí se vieron asociadas a una disminución significativa en paralelo de la PAPm/IC durante la AAO2 99.5%. Observaciones hemodinámicas que para la cohorte A, se caracterizaron por una reducción de la PAPm promedio (12.3 mmHg, p <0.004), por una disminución de la Sp de 6.02; 95% CI: 4.04 - 8 a 4.3; 95% CI: 4.11 - 4.49 mmHg/L min/m², (p <0.008) y por el descenso de Pext de 8.58 ± 3 a 4.7 ± 1.4 mmHg, p <0.01, al compararse con las documentadas RAA. En cambio, para la cohorte B, la PAPm promedio y la PAPm/IC no se modificaron, Sp mostró sólo tendencia a disminuir (p = 0.08) y Pext aumento de 12 ± 2.9 a 20.6 ± 4.9 mmHg, (p <0.03) en relación a las registradas RAA. Bajo la AAO2 - 99.5%, se observaron diferencias significativas para la PAPm/ IC - 95% IC en su localización, para la PAPm promedio (A: 19.5 ± 6 vs. B: 41.2 ± 11.5 mmHg, p <0.001) y Pext (A: 4.7 ± 1.4 vs. B: 20.6 ± 4.9 mmHg, p <0.001) y sin cambios en la Sp, entre la cohorte A y la B. Conclusiones: Cuando se analiza la PAPm/IC, se obtiene información que es valiosa para interpretar la resistencia vascular pulmonar linear en sujetos con EPOC e H P. Sin embargo, las anormalidades de la PAPm/IC, no necesariamente reflejan aumento exclusivo de la resistencia arteriolar pulmonar para sujetos con EPOC e H P. De acuerdo con las observaciones agudas de este estudio, posiblemente solo sea de esperarse beneficio con la oxigenoterapia a largo plazo sobre la circulación pulmonar y la post-carga del ventrículo derecho, para aquellos portadores de EPOC e HP cuando la PAPm en el reposo sea <30 mmHg.

Left and right ventricular power: outputs are the strongest hemodynamic correlates to allow identification of acute responders to vasodilator treatment in idiopathic pulmonary arterial hypertension / El poder del ventrículo derecho y del izquierdo: son parámetros hemodinámicos que correlacionan con la posibilidad de ser respondedor durante el reto agudo con vasodilatadores en la hipertensión arterial pulmonar idiopática

Introduction: Despite the prognostic importance of traditionally derived measurements, the significance of right heart catheterization (RHC) remains controversial. Thus, a continued search for hemodynamic markers that define better responsive patients is required. Since, right ventricular failure is the most fatal pathway, right (RVPO) and left (LVPO) ventricular power output are parameters that could provide input for a better understanding of the hemodynamics involved in idiopathic pulmonary artery hypertension (IPAH). Method: We retrospectively analyzed how demographics and outcome correlate with hemodynamics to identify responders among IPAH patients. Results: Ninety patients fulfilled the following criteria for inclusion in this study: (1) complete RHC at baseline; (2) an acute evaluation for vasodilators (AEFV, including a positive response, that is, an increase in CO, a decrease in both mPAP and pulmonary vascular resistance ≥ 20% from baseline, respectively); and (3) a long-term follow-up under accepted IPAH treatments. If RVPO decreased (p < 0.001) and LVPO increased (p < 0.012) during AEFV, it is considered that these findings reinforce our ability to identify responders; that is, patients that remained as responders after 6.4 ± 3 years under nifedipine treatment (37.7% of the studied IPAH population). After multivariate analysis, age, RVPO, and LVPO remained as independent variables (OR = 0.927, 95%CI: 0.87-0.98, p = 0.01; OR = 0.114, 95%CI: 0.00-0.91, p = 0.045; and OR = 171.5, 95% CI: 5.3-549, p = 0.004, respectively) when estimating the probability of being a responder. On this basis, an equation was derived to identify responders among IPAH patients, where the probability of being a responder = 1.0196-0.0631 (age) - 4.7693 (RVPO) + 3.8152 (LVPO), ROC: 0.76, 95% CI: 0.63-0.89; p = 0.001. Conclusion:based on the proposed equation, LVPO and RVPO could be used for the identification of responders among IPAH patients.

Introducción: A pesar de la importancia y del significado pronóstico que tienen las mediciones directas y las derivadas del cateterismo cardiaco derecho, éstas permanecen hasta el día de hoy en el terreno académico de la controversia. Por lo tanto, se requiere la continua búsqueda de marcadores hemodinámicos para estratificar a los enfermos con hipertensión arterial pulmonar idiopática. Particularmente, cuando la disfunción contráctil del ventrículo derecho es la vía final más común de esta patología. En esta circunstancia, la determinación del poder del ventrículo derecho y del ventrículo izquierdo representa parámetros que pudieran ser de utilidad para lograr un mejor entendimiento en la hemodinámica de la hipertensión arterial pulmonar idiopática. Método: De manera retrospectiva, analizamos los aspectos demográficos, los hemodinámicos y la sobrevivencia, y si éstos se vieron asociados a la posibilidad de ser enfermos respondedores entre los portadores de hipertensión arterial pulmonar idiopática. Resultados: Noventa enfermos llenaron los siguientes criterios para ser incluidos en el estudio: 1. Contar con cateterismo cardiaco derecho basal; 2. Tener valoración aguda con adenosina, en donde quedó definida una respuesta "positiva aguda" como: aumento del gasto cardíaco, disminución de la presión arterial pulmonar media y de la resistencia vascular pulmonar calculada (≥ 20% de la basal, respectivamente) y; 3. Contar con un seguimiento a largo plazo bajo la influencia de los tratamientos modernos aceptados para enfermos con hipertensión arterial pulmonar idiopática. Sí, el poder del ventrículo derecho disminuyó (p < 0.001) y el poder ventrículo izquierdo aumentó (p < 0.012) durante el reto vasodilatador agudo se consideró que éstos hallazgos reforzaban la habilidad para detectar a los sujetos respondedores con hipertensión arterial pulmonar idiopática; población de enfermos que guardó ese comportamiento hemodinámico durante 6.4 ± 3 años bajo la influencia de nifedipina (37% de la totalidad de la población con hipertensión arterial pulmonar idiopática). Después de efectuar un análisis multivariado, la edad, el poder del ventrículo derecho y del ventrículo izquierdo permanecieron como variables independientes (OR = 0.927, 95%IC: 0.87-0.98, p = 0.01; OR = 0.114, 95%IC: 0.00-0.91, p = 0.045; y OR = 171.5, 95%IC: 5.3-549, p = 0.004, respectivamente) para ser considerados "respondedores". Como resultado, se derivó una ecuación donde la probabilidad de ser respondedor = 1.0196-0.0631 (edad) - 4.7693 (poder del ventrículo derecho) + 3.8152 (poder del ventrículo izquierdo), ROC: 0.76, 95%CI: 0.63 - 0.89; p = 0.001. Conclusión: Con fundamento en los hallazgos de este estudio, la ecuación propuesta, el poder del ventrículo derecho y el ventrículo izquierdo pueden ser utilizados para identificar "respondedores" entre los enfermos con hipertensión arterial pulmonar idiopática.

Interpretación de la relación presión-flujo en la hipertensión arterial pulmonar idiopática / Pressure-flow relationships interpretation in idiopathic pulmonary arterial hypertension

Objetivo: Conocer más de la relación presión arterial pulmonar media/índice cardiaco y sus perfiles en enfermos con hipertensión arterial pulmonar idiopática. Métodos: La presión arterial pulmonar media/índice cardiaco y la presión extrapolada al eje de cero flujo se obtuvo en 40 enfermos respirando aire ambiente, oxígeno 99.5% e hidralazina. Se obtuvieron dos grupos de acuerdo a criterios de "respuesta vasodilatadora aguda", respondedores (n = 20) y no respondedores (n = 20). Se analizó este criterio versus el propuesto por la Task Force de la Sociedad Europea de Cardiología en la población respondedora. Resultados: La presión arterial pulmonar media/Índice cardiaco se ubicó de forma anormal en el diagrama de presión-flujo de la cohorte total, (p < 0.01). Sin alteraciones en el intercambio gaseoso o mecánica pulmonar. Para los enfermos respondedores versus no respondedores, la pendiente fue anormal 2.2 (95%IC:1.1-3.3) vs. 5.89 (95%IC:4.69-7.11) mm Hg/L min/m² e incremento de la presión extrapolada al eje de cero flujo (38.2 ± 7.5 a 66.3 ± 7.5 mm Hg, p < 0.01). Sin diferencias con oxígeno al 99.5%. Con vasodilatador, la presión arterial pulmonar media disminuyó (52.1 ± 9.5 a 40 ± 5.5 mm Hg, p < 0.01) vs. no se modificó (96.2 ± 8.5 vs. 90 ± 7.5 mmHg, p = 0.3), pendiente 1.15 (95%IC:0.68-1.62) vs. 1.28 (95%IC:0.78-1.78) mmHg/Lmin/m², la presión extrapolada al eje de cero flujo no cambió vs. incrementó (69.4 ± 7.8 a 85.1 ± 8.5 mm Hg, p < 0.01), en relación al control. En no respondedores con vasodilatador, la presión arterial pulmonar media/índice cardiaco (90 ± 7.5 mmHg, pendiente:1.28; 95%IC: 0.78 - 1.78 mm Hg/L min/m²) fue diferente al comparar respondedores con menor o mayor de 40 mm Hg de presión arterial pulmonar media. Presiones 34 ± 3 vs. 45 ± 4 mm Hg y pendientes 1.14 (95%IC: 0.67 -1.61 vs. 2.22 (95%IC: 1.35 - 3.09 mm Hg/L min/m²), respectivamente p < 0.01. Conclusiones: Las anormalidades de la relación presión arterial pulmonar media/Índice cardiaco reflejan el incremento de las resistencias vasculares pulmonares reales a nivel arteriolar pulmonar en enfermos con hipertensión arterial pulmonar idiopática. Ambos criterios de respuesta vasodilatadora aguda son de utilidad para identificar respondedores y no, en esta población de enfermos.

Objectives: We analyze exercise-derived mean pulmonary artery pressure/cardiac index relationship to expand the concepts regarding its nature and to better identify "responders" in idiopathic pulmonary arterial hypertension patients. Methods: Mean pulmonary artery pressure/cardiac index relationship and extrapolated pressure to zero flow were obtained in 40 patients' breathing room air, oxygen 99.5% and hydralazine. The hemodynamic characteristics were analyzed for the cohort and separate for responders (n = 20) and non responders (n = 20) according to the acute response to vasodilator. We tested this previous criteria versus the Task Force on diagnosis and treatment prescribed by the European Society of Cardiology. Results: The mean pulmonary arterial pressure/cardiac index was located abnormally in the pressure-flow diagram of the total cohort (p < 0.01). No alterations in gas exchange or lung mechanics. For patients responders versus non-responders, the slope was abnormal 2.2 (95% CI:1.1-3.3) vs. 5.89 (95% CI: 4.69 - 7.11), mm Hg/L min/m² and increased extrapolated pressure to zero flow (38.2 ± 7.5 to 66.3 ± 7.5 mm Hg, p <0.01). Without difference with oxygen 99.5%. With vasodilator effect, mean pulmonary arterial pressure decreased (52.1 ± 9.5 to 40 ± 5.5 mm Hg, p <0.01) versus it did not change (96.2 ± 8.5 versus 90 ± 7.5 mm Hg, p=0.3), slope 1.15 (95% CI: 0.68 - 1.62) vs. 1.28 (95% CI: 0.78-1.78) mmHg/L min/m², the extrapolated pressure to zero flow did not change (69.4 ± 7.8 to 85.1 ± 8.5 mm Hg), p <0.01, compared to control. In non-responders with vasodilator, mean pulmonary arterial pressure/cardiac index (90 ± 7.5 mmHg, slope: 1.28, 95% CI :0.78 - 1.78 mm Hg/L min/m²) was different between responders < or > 40 mmHg mean pulmonary arterial pressure. Pressures were 34 ± 3 vs. 45 ± 4 mm Hg and slopes 1.14 (95% CI: 0.67 - 1.61) vs. 2.22(95% CI: 1.35 - 3.09) mm Hg/L min/m², p <0.01, respectively.. Conclusions: Abnormalities of the mean pulmonary arterial pressure/cardiac index relationship exercise-derived seems to reflect "mainly arteriolar" increased lineal pulmonary vascular resistance in idiopathic pulmonary arterial hypertension patients. Both acute vasodilator response criteria are useful to identify responders and not responders in this patient population.

Interpretación clínica de la relación presión-flujo en enfermos con alveolitis alérgica extrínseca con neumopatía intersticial crónica e hipertensión pulmonar: ¿debemos tratar la hipertensión, la patología pulmonar o ambas? / Clinical interpretation for the pressure-flow relationships in extrinsic allergic alveolitis and in interstitial lung disease pulmonary hypertension patients: should we care for the lung, the pulmonary artery pressure or both?

OBJECTIVES: We sought to analyze exercise-derived mean pulmonary artery pressure (mPAP)-cardiac index (CI) relationship to expand the concepts regarding its nature and to better identify pulmonary hemodynamic responders to acute oxygen breathing (AO2B-99.5%) and to hydralazine (H) in extrinsic allergic alveolitis (EAA) and chronic interstitial lung disease (CILD) pulmonary hypertension (PH) patients. MATERIAL AND METHODS: mPAP/CI and extrapolated pressure (Pext) to zero flow were obtained while breathing room air (BRA) and under AO2B-99.5% in 38 stable (EAA (n = 14) and CILD (n = 24)) patients with resting and exercising PH. Hemodynamic characteristics were analyzed for the entire cohort and separate for EAA and CILD patients. AO2B-99.5% was tested in cohorts, H only in CILD and the effect of long-term corticosteroid treatment in EAA patients. Lung biopsies (LB) were obtained to evaluate the inflammatory-fibrosis stage and the degree of vascular lesion in the entire cohort. RESULTS: LB studies reveal a predominant stage of inflammation associated with grade-I vascular lesion for EAA patients. A predominant stage for fibrosis (although moderate) over inflammation associated with grade-II vascular lesions were documented for CILD patients. mPAP/CI abnormal location were associated with hypoxemia/decreased mixed venous-PO2 and lung mechanics abnormalities for both cohorts. An abnormal slope (Sp: 4.13; 95% CI: 3.42-4.84 mmHg/L/min/m2) and a normal Pext value (7 +/- 1.9 mmHg) were found for EAA patients. On the contrary, a normal slope (Sp: 1.22; 95% CI: 0.47-1.99 mmHg/L/min/m2) and an abnormal Pext value (19.7 +/- 3.5 mmHg) were found for CILD patients. Hemodynamic conditions that did not change for the Sp (4.0; 95% CI: 3.18-4.82 mmHg/L/min/m2); however, were associated with a statistical significant decrease in parallel for mPAP/CI during AO2B-99.5% when compared to BRA (p < 0.01), although not to normal slope values (0.96; 95% CI: 0.41-1.37) or mPAP/CI location. For CILD patients, during AO2B-99.5% no change for the slope, for Pext and mPAP/CI location in relation to BRA were observed. Under the effect of H, no change for the previous mentioned hemodynamic findings were found in relation to the control condition for CILD patients. After long-term corticosteroid treatment, normalization for mPAP/CI location and for the slope value (1.6; 95% CI: 0.91-2.29 mmHg/L/min/m2) were associated with lung mechanics and blood-gas exchange normalization were document...

A proposed functional clinical classification predicts in-hospital and long-term survival in the setting of acute right ventricular infarction / Propuesta de una clasificación funcional y clínica para predecir la sobrevida intrahospitalaria y a largo plazo de enfermos con infarto agudo del ventrículo derecho

BACKGROUND: The objectives of the present investigation were to validate the prognostic role of a proposed Clinical Classification [CC], to evaluate the TIMI risk score [RS] and to establish whether the TIMI-RS should incorporate points for patients with acute right ventricular infarction [TIMI-RS-RVI]. METHODS AND RESULTS: A total of 523 RVI patients were classified on clinical and functional basis as: A, without right ventricular failure [RVF], B with RVF and C with cardiogenic shock. The CC was evaluated prospectively among 98 patients with RVI and retrospectively in 425 RVI patients. The TIMI-RS was evaluated prospectively among 622 patients with STEMI [anterior:277, inferior:247, RVI:98], and retrospectively in 425 RVI patients. The CC established differences among the 3-RVI Classes for in-hospital mortality [prospectively and retrospectively; p<0.01, p<0.001, respectively] that were maintained at 8 years [p < 0.001]. Patients with anterior and inferior STEMI, but not those with RVI revealed an association between outcome and TIMI-RS [p<0.001]. Testing for TIMI-RS-RVI did not result a good prognostic tool [ROC=0.9; excellent discrimination, but with a very poor [quot ]clinical calibration[quot ]]. CONCLUSIONS: The proposed CC allowed prediction of mortality at short- and long-term in the setting of acute RVI. The role of the TIMI-RS should be reevaluated prospectively as a prognostic tool in the scenario of RVI patients.

La autorregulación homeométrica: el efecto Anrep: su posible importancia en la patofisiología en los aumentos de la postcarga del ventrículo derecho / Homeometric autoregulation in the heart: the Anrep effect: its possible role in increased right ventricular afterload pathophysiology

One type of intrinsic response exhibited by the isolated and non-isolated heart is the well-known Frank-Starling mechanism, which endows the ventricles with performance characteristics such that the heart ejects whatever volume is put into it [heterometric autoregulation]. A second type of autoregulation in the isolated and no-isolated heart, one which apparently does not utilize the Frank-Starling mechanism, will be the main subject of this review. It requires at least a few beats to develop fully after an increase in activity. The ventricle then exhibits performance characteristics such that its end-diastolic pressure and fiber length tend to be maintained because of an increase in myocardial contractility. It will, therefore be referred to as homeometric autoregulation or Anrep effect. Assessment of ventricular load-independent parameters, including myocardial contractility, is important to better understand the pathophysiology of acute and right ventricular increased afterload. The role of the Anrep effect, in right ventricular dysfunction in patients with primary or secondary forms of pulmonary artery hypertension with chronic cor pulmonale, is analyzed and presented as an hypothesis to be considered in the pathophysiology in acute and in chronic states of right ventricular afterload.

Optimización de los recursos de la imagenología en la cardiopatía isquémica / Staging imagenology in coronary syndromes

For the physician, it should stand out very clearly that the clinical and rationale analysis of the symptoms observed in every patient suffering from stable chronic ischemic cardiopathy (SCIC) or acute coronary ischemic syndrome (ACIS), are the starting point to apply the available resources in imagenology, in order to apply in an optimized and sequential manner to stratify, without forgetting its inherent limitations, or identify its risk. This approach may be based on the ethics, with special emphasis on the patient economy, which may promote the use of indissoluble medical principles regarding never damaging, but improving, the survival. SCIC and ACIS prevalence is still very high in its actually recognized clinical-pathological avenues.

De la reperfusión al post-acondicionamiento del miocardio con isquemia prolongada. Nuevo paradigma terapéutico de los síndromes coronarios agudos con elevación del segmento ST? De lo básico a lo clínico / Reperfusion and postconditioning in acute ST segment elevation myocardial infarction. A new paradigm for the treatment of acute myocardial infarction. From bench to bedside?

After prolonged periods of ischemia and energy depletion, the ischemic myocardial cell can be jeopardized by specific causes within the reperfusion period. These causes can be viewed as unwanted aspects of the recovery process itself limiting its efficiency. Three potential initial causes of immediate reperfusion injury, aside from oxygen radicals, have been experimentally investigated in detail, and are briefly discussed: 1. re-energization; 2. rapid normalization of tissue pH; and 3. rapid normalization of tissue osmolality. These potential causes are not entirely independent. Understanding of the basic causes has opened novel perspectives for specific interference with these serious pathomechanisms. The experimental results obtained in the last years encourage the development of therapeutic approaches to reduce infarct size by specific measures applied during the early phase of reperfusion. In the clinical setting, reperfusion therapy for acute myocardial infarction (AMI) has shown to reduce mortality, yet it may also have deleterious effects, including myocardial necrosis and no-reflow. Almost two decades ago, great hope arose from the description of ischemic preconditioning. Unfortunately, ischemic preconditioning is not feasible in the clinical practice because the coronary artery is already occluded at the time of hospital admission of the AMI patient. Recently, in the dog model, a phenomenon called [quot ]postconditioning[quot ] has been described. It has been reported previouly that reperfusion injury can be significantly reduced by modifying the conditions and the composition of the initial reperfusate. Whereas preconditioning is triggered by brief episodes of ischemia-reperfusion performed just before a prolonged coronary artery occlusion, postconditioning is induced by a comparable sequence of reversible ischemia-reperfusion, but it is applied [quot ]just after the prolonged[quot ] ischemic insult. Protection afforded by postconditioning is as potent as that provided by preconditioning. Unlike preconditioning, the experimental design of postconditioning allows direct application in the clinical practice, especially during PTCA. It has been reported very recently, that postconditioning patients with ST segment elevation AMI, during coronary angioplasty protects the human heart in this clinical scenario. Obtaining such a beneficial effect by a simple manipulation of reperfusion is of major potential clinical interest. Now more than ever,

Estratificación clínica del enfermo con estado de choque cardiogénico, el valor agregado del poder cardíaco y del índice de las resistencias periféricas / Clinical stratification of cardiogenic shock

Cardiogenic shock (CHC) associated to acute myocardial infarct has high mortality and their manifestations are heterogenous. In our institution historical mortality, was 98%, but with different methods of reperfusion, its reduced to 53%. In other hand, with opportune clinical stratification is useful to improve the treatment strategy. This stratification on basis in clinical signs: age, infarction location, cardiac frequency and systemic arterial pressure, and hemodynamical valuation with the use of right catheterism with quantification miocardial work parameters like [quot ]Cardiac power[quot ] that is the product of flow and arterial pressure and that is of utility to know the [quot ]Miocardial reserve[quot ]. In our experience after reperfusion procedure patients with CHC and cardiac power less than 1.0 had highly mortality.

De la placa vulnerable solitaria, a la coronariopatía de múltiples vasos. De sus fundamentos, a las implicaciones terapéuticas modernas. Una realidad clínica en el espectro de los SICA / From the single vulnerable plaque, to the multiple complex coronary plaques. From their basis, to the modern therapeutic approach. A clinical reality in the spectrum of the acute coronary syndromes

Contemporary clinical and laboratory data have challenged our classical concepts of the pathogenesis of the acute coronary syndromes [ACS]. Indeed, several independent lines of clinical evidence have supported that the critical stenoses cause only a fraction of the ACS. Acute myocardial infarction is believed to be caused by rupture of a vulnerable coronary-artery plaque that appears as a single lesion on angiography. However, plaque instability might be caused by pathophysiologic processes, such as inflammation, that exert adverse effects throughout the coronary vasculature and therefore result in multiple unstable lesions. Recent studies have demonstrated that ruptured or vulnerable plaques exist not only at the culprit lesion but also in the whole coronary artery in some ACS patients. It has also been reported that a ruptured plaque at the culprit lesion is associated with elevated C- reactive protein and other inflammatory markers, which indeed indicate a poor prognosis in patients with ACS. Also, multiple plaque rupture is associated with systemic inflammation, and patients with multiple plaque rupture can be expected to show a poor prognosis. Therefore some ACS patients [20-40%] may harbor multiple complex coronary plaques that are associated with adverse clinical outcomes. It should be accepted that this ACS population represent a part of the spectrum of the ACS, and in particular in this group of patients treatment should focus not only on the stabilization of the culprit site but also warrants a broader approach to systemic stabilization of the arteries. However, recurrent cardiovascular events in this population still remain unacceptably high, indicating that plaque rupture or vulnerability of multiple plaques is a current challenge in the management of ACS patients.

De la placa vulnerable solitaria, a la coronariopatía de multiples vasos. De sus fundamentos, a las implicaciones terapéuticas modernas. Una realidad clínica en el espectro de los SICA / From the single vulnerable plaque, to the multiple complex coronary plaques. From their basis, to the modern therapeutic approach. A clinical reality in the spectrum of the acute coronary syndromes

Contemporary clinical and laboratory data have challenged our classical concepts of the pathogenesis of the acute coronary syndromes [ACS]. Indeed, several independent lines of clinical evidence have supported that the critical stenoses cause only a fraction of the ACS. Acute myocardial infarction is believed to be caused by rupture of a vulnerable coronary-artery plaque that appears as a single lesion on angiography. However, plaque instability might be caused by pathophysiologic processes, such as inflammation, that exert adverse effects throughout the coronary vasculature and therefore result in multiple unstable lesions. Recent studies have demonstrated that ruptured or vulnerable plaques exist not only at the culprit lesion but also in the whole coronary artery in some ACS patients. It has also been reported that a ruptured plaque at the culprit lesion is associated with elevated C- reactive protein and other inflammatory markers, which indeed indicate a poor prognosis in patients with ACS. Also, multiple plaque rupture is associated with systemic inflammation, and patients with multiple plaque rupture can be expected to show a poor prognosis. Therefore some ACS patients [20-40%] may harbor multiple complex coronary plaques that are associated with adverse clinical outcomes. It should be accepted that this ACS population represent a part of the spectrum of the ACS, and in particular in this group of patients treatment should focus not only on the stabilization of the culprit site but also warrants a broader approach to systemic stabilization of the arteries. However, recurrent cardiovascular events in this population still remain unacceptably high, indicating that plaque rupture or vulnerability of multiple plaques is a current challenge in the management of ACS patients.

El poder cardíaco un instrumento del pasado, posiblemente una herramienta moderna en la valoración: clínica, terapéutica y pronóstica del choque cardiogénico por síndrome isquémico coronario agudo / The cardiac power output an old tool, possibly a modern tool for assessing cardiac pumping capability, as well as for a short-term prognosis in cardiogenic shock due to acute myocardial infarction

Hemodynamic monitoring has been used extensively during the last decades for risk stratification and guiding treatment of patients with cardiovascular destabilization, especially in the scenario of acute heart failure and cardiac shock. Every cardiac pump has its own maximum performance, which denotes its pumping capability. The heart is a muscular mechanical pump with an ability to generate both flow (cardiac output) and pressure. The product of flow output and systemic arterial pressure is the rate of useful work done, [quot ]or the cardiac power[quot ] (CP). Cardiac pumping capability can be defined as the cardiac power output achieved by the heart during maximal stimulation, and cardiac reserve is the increase in power output as the cardiac performance is increased from the resting to the maximally stimulated state (CPR). Resting CP for a hemodynamically stable average sized adult is approximately 1 W. However, during stress or exercise, CPR can be recruited to increase the heart's pumping ability up to 6 W. In acute heart failure, the patient becomes hemodynamically unstable, and most of the cardiac pumping potential is recruited in order to sustain life. Hence, cardiac power measurements in patients with acute heart failure or with cardiogenic shock at rest represent most of the recruitable reserve available during the acute event, and their measurement reflects the severity of the patient's condition. It has been found that a cutoff value for CP of 0.53 W accurately predict in-hospital mortality for cardiogenic shock patients. Others investigators observed cutoff for increased mortality of CP < 1 W, data that were obtained at doses of maximal pharmacologic support yielding the individual maximal CP. In our experience, the cutoff value for CP that accurately predicts in-hospital mortality for cardiogenic shock patients is 0.7 W, but its impact on short-term prognosis is clearer if the patient achieves a CP equal or higher than 1 W after an optimal myocardial revascularization with interventional cardiac procedures. According to the data collected from the literature, CP deserves a place in the evaluation of the patient with cardiogenic shock due to an acute myocardial infarction, but a more profound analysis of this parameter an further evaluation are required in order to better understand its prognostic meaning in this acute cardiac syndrome.

Choque cardiogénico: Las variables de mortalidad / Mortality in cardiogenic shock

Objetivo: El choque cardiogénico (CHC) es la causa más frecuente de mortalidad después de un infarto agudo del miocardio (IAM). El objetivo de este trabajo fue conocer cuáles son las principales variables de mortalidad del CHC. Métodos: Se estudiaron en período consecutivo de 12 años a 155 enfermos del Servicio de Urgencias del Instituto Nacional de Cardiología "Ignacio Chávez ". Resultados: En los enfermos mayores de 60 años con antecedentes de diabetes mellitus y con cardiopatía isquémica la mortalidad fue mayor (p<0.001). Al analizar los procedimientos terapéuticos, el grupo de tratamiento exclusivamente médico (n=79) tuvo mortalidad de 97.4% y el de revascularización temprana (n=76) de 59.2% con diferencia significativa (p<0.001). Conclusiones: Se concluye que el CHC tiene mortalidad elevada (78.7%) en el grupo global; que la edad, la presencia de diabetes y el antecedente de cardiopatía isquémica empeoran su pronóstico, y que la revascularización temprana como método terapéutico disminuye su mortalidad.

Objective: Cardiogenic shock (CS) is one of principal causes of mortality after an acute myocardial infarction (MI). The objective of this study was to determine the principal causes that contribute to an increase in mortality in CS. Methods: We studied 155 consecutive patients with CS admitted to the Coronary Care Unit of the Instituto Nacional de Cardiología Ignacio Chávez from 1990 2002. Results: Patients older than 60 years with MI and diabetes mellitus presented a higher cardiovascular mortality (p<0.001). Percutaneous coronary intervention (PCI) procedures decreased the cardiovascular mortality in CS as compared to those patients not submmitted to PCI (59% vs. 98%, p<0.001). Conclusions: Mortality due to CS is still very high (80%). Previous MI and diabetes favor short term mortality and the use of PCI suggests a clinical favourable trend in the reduction of mortality due to CS. PCI appears to be the most appropriate reperfusion procedure for treating CS.

La meta de la reperfusión en los síndromes isquémicos coronarios agudos con elevación del segmento ST. El gran paradigma: "Lo que hay más allá del flujo TIMI 3 epicárdico: El TIMI 4 miocárdico" / The target of reperfusion in ST - elevation acute coronary syndromes: The major paradigm: "beyond TIMI 3 flow: The TIMI 4 or myocardial tissue - level perfusion"

En el tratamiento de los Síndromes Coronarios Agudos con elevación del segmento ST se ha avanzado en la última década de manera favorable en relación a la terapia fibrinolítica (TF), en los procedimientos coronarios intervencionistas (PCI) y con la utilización concomitante de los inhibidores de los receptores plaquetarios IIb/IIIa (IRP). El interés actual en relación al objetivo ha alcanzar en la reperfusión del infarto agudo del miocardio (IAM) ha girado de la arteria responsable del infarto (ARI) a obtener perfusión microvascular-tisular óptima. Se ha puntualizado que el establecer la mejor permeabilidad de la ARI (TIMI 3E) no es sinónimo de que también se ha obtenido en el tejido miocárdico (TIMI 4 M). Sabemos que puede existir disfunción microvascular producto de la microembolización plaquetaria o la ocasionada por la propia reperfusión, misma que esta ligada a los mediadores inflamatorios lo que da origen al "fenómeno de no- flujo", anomalía todas que ocurren en un número no despreciable de enfermos a pesar de haberse obtenido TIMI 3E. Hoy día hay técnicas y tratamientos que van encaminados a identificar y resolver estas anomalías con el fin de mejorar la perfusión microvascular en el IAM. A pesar de existir progresos en las estrategias de reperfusión en el IAM particularmente con el empleo adjunto de IRP y con la TF y que se obtienen en la ARI flujos TIMI 3E en el 50-75% de las veces y con los PCI en el 90-95%, no se han alcanzado reducciones significativas en la mortalidad, mas sí en la frecuencia de la retrombosis de la ARI, de los stents, de reinfartos y en algunos sujetos se observa mejoría de la función ventricular. Por lo tanto, hoy día estamos conscientes de lo que representa obtener perfusión óptima microvascular en el escenario del IAM. El gran paradigma es saber por lo tanto que hay más allá del TIMI 3E y si se alcanzo o no flujo TIMI 4 o miocárdico.

Treatment for ST- elevation acute coronary syndromes (acute myocardial infarction: AMI) has advanced rapidly in the last decade with major improvements in early fibrinolytic therapy (FT), primary percutaneous interventions (PCI) with the aid of platelet glycoprotein IIb/IIIa inhibitors. Recent interest has shifted from infarct related artery (IRA) patency to microvascular perfusion in the evaluation of patients with AMI. It is well known that establishing epicardial patency after AMI (TIMI 3 E) is not synonymus with tissue-level perfusion (TIMI 4M). Microvascular dysfunction due to the roles of platelet and inflammatory mediators in the no-reflow phenomenon occurs in a substancial proportion of patients despite thrombolytic therapy or PCI procedures. Techniques are now available that measure real tissue-level perfusion and also therapy is directed to optimize myocardial perfusion in patients with AMI. Despite advances, contemporary FT strategies with the combination of platelet glycoprotein IIb/IIIa inhibitors restore normal coronary flow (TIMI 3) in the IRA in only 50-75% and PCI achieves TIMI 3 flow rates in 90-95%, but only with modest reductions in mortality, but with significant reductions in rethrombosis of the IRA or stents, reinfarctions and in some patients with benefits in ventricular dysfunction. Therefore moving beyond the importance of TIMI 3 flow, the TIMI 4 flow, or improving tissue-level perfusion in the setting of AMI seems to be the paradigm for the treatment of ST-elevation acute coronary syndromes.

Infarto agudo del ventrículo derecho. Fisiopatología-tratamiento y pronóstico / Right ventricular infraction. Pathophysiology-treatment and prognosis

Se revisa la fisiopatología, el cuadro clínico y el tratamiento del infarto agudo del ventrículo derecho (IAVD). Aunque los estudios no invasivos han demostrado dilatación y anormalidades de la contracción ventricular derecha en del 50 por ciento de los enfermos con esta patología, sólo ocurren alteraciones hemodinámicas significativas en la mitad de ellos. Cuando se identifican enfermos con IAVD se debe clasificar como Clase A: aquellos sin disfunción ventricular derecha (DVD), Clase B: con DVD y Clase C: en estado de choque. La terapia trombolítica (TT) o los procedimientos cororarios intervencionistas (PCI) debe aplicarse siempre de no estar contraindicados ya que se observó con ellos tendencia a disminuir la mortalidad. En la clase B (la TT o los PCI) reducen la DVD, en la clase C la TT luce sin beneficio y los PCI abaten la mortalidad.

La influencia del pericardio en la patofisiología de la disfunción ventricular en el infarto agudo del ventrículo derecho: estudio experimental / The role of the pericardium in the pathophysiology of ventricular dysfunction in experimental acute right ventricular infarction

Para obtener mayor información de la función del pericardio en el Infarto Agudo del Ventrículo Derecho (IAVD) se estudiaron las curvas de función ventricular (CFV) y la relación de las presiones diastólicas finales ventriculares (R-Pd2V, VD: VI) en un modelo canino. Estos se dividieron en: Grupo A (N = 12): Basal (B), IAVD, Postpericardiectomía (PP). La CFV derecha (D) B se comportó como parábola y su punto de flexión (PF) estuvo en 13 ñ 2 mmHg de Pd2V. En el IAVD la CFVD se ubicó abajo y a la derecha de la CFVD B (p < 0.05) y el PF se desplazó a 18 ñ 2 mmHg p < 0.05), PP la CFVD se desplazó arriba y a la izquierda de la CFVD IAVD (p = NS). La R- Pd2V VD: VI B fue: 0.75, en IAVD: 0.91 y PP: 0.84 (p = NS). Grupo B (N = 12): Basal (B), Postpericardiectomía (PP) e IAVD. La CFVD PP se desplazó arriba y a la izquierda de la CFVD B (p < 0.05) y el PF fue = 10 ñ 2 mmHg. En IAVD la CFVD se ubicó abajo y a la derecha de la CFVD PP (p < 0.05) y la R-Pd2V, VD:VI fue de 0.45 PP, y con el IAVD se igualaron (0.95) significativamente (p < 0.05). Conclusiones: En la génesis del gasto cardiaco (GC) bajo del IAVD se demostró el papel restrictivo parcial del pericardio, ya que la igualdad de la R-Pd2V se debe también a isquemia. El PF de la CFVD con IAVD (18 + 2 mmHg) es la cifra límite para la infusión de volumen en el IAVD experimental. A reserva de validarse en el hombre este dato puede ser útil para el manejo de la precarga en el humano con IAVD e hipotensión sistémica o GC bajo.