[Clinical-hemodynamic correlation of the NYHA/WHO system in idiopathic pulmonary artery hypertension. Clinical, therapeutic and long-term prognosis implications]. / Correlación clínica-hemodinámica de la clasificación de la NYHA4/WHO en enfermos con hipertensión arterial pulmonar idiopática. Sus implicaciones en la clínica, en el tratamiento y en el pronóstico a largo plazo.

BACKGROUND: The most often used functional classification for categorizing the degree of cardiac disability in patients with chronic left ventricular failure is the NYHAN/WHO system. In Idiopathic Pulmonary Arterial Hypertension [I-PAH], this system although used, has not been studied in detail regarding pulmonary hemodynamic parameters association and for long-term prognosis in each of the NYHA/WHO classes. METHODS: We retrospectively, studied the NYHA/ WHO system in 83 I-PAH patients. Patients were separated according to the response in the acute vasodilator trial in responders [n = 30] and nonresponders [n = 53]. RESULTS: Classes I - II did not represent the minority population for I-PAH patients [58/83 = 60%]. Only mean right atrial pressure [mRAP] and mean pulmonary artery pressure [mPAP] were different among the NYHA/WHO functional classes [p < 0.000 and p <0.012; respectively]. I-PAH patients class I have the probability to be a responder 12.6 times more [CI 95.%: 4.59-40.62; p < 0.000]. The long-term mortality for class I patients was 0.%, for class II: 2.%, for class III: 28.% and for class IV: 63.% [p < 0.0001]. The follow-up change for one grade class of the NYHA/WHO classes at four years was noticed only in 20.% of the I-PAH patients. CONCLUSIONS: NYHA/WHO classes I-II did not represent the minority of I-PAH patients population as has been previously considered. Only mRAP and mPAP were different among the NYHA/WHO classes. The NYHA/ WHO system on the basis of mRAP and mPAP allows to separate classes I-II from III-IV. I-PAH patients class I have 12.6 times more the probability to be a responder and better long-term survival; irrespective of the treatment the prognosis seems to be excellent for this functional class group patients.

[Calculated pulmonary vascular resistance, is definitively a worthless variable. Current methods for a better definition]. / La resistencia vascular pulmonar "calculada". Un parámetro incierto para la valoración de la circulación pulmonar. Los métodos actuales para determinarla.

The term pulmonary vascular resistance [PVR] describes, in part, the forces opposing the flow across the pulmonary vascular bed. The equation traditionally used is based on the assumption that the pulmonary capillaries, as well as some others vessels in series behave like a Poiseuille resistance. This assumption implies a laminar type of flow of a homogeneous Newtonian fluid, however blood is not a Newtonian fluid and flow is pulsatile in the pulmonary circulation. Neglecting these factors [which only slightly undermines the application of the equation] and others as well [like distension and recruitment of the vessels], will, however, not give us a true clinically practical solution for the calculation of PVR, because the concept of the equation is only true or partially true for part of the pulmonary circulation. In other parts of the lung, flow depends mainly on the behaviour of capillaries as a Starling resistor. If we considered always pulmonary venous pressure [measured clinically as left atrial pressure or pulmonary wedge pressure] as the effective downstream pressure for the calculation of PVR and we ignore or disregard the existence of a significant "critical closing pressure" [whatever the cause] in the lung it will lead to additional erroneous concept regarding PVR calculations and, in addition for the real hemodynamic conditions of the pulmonary vascular bed. Because, at least two different models of perfusion exist in the lung it is inadmissible from a theoretical point of view to calculate PVR, based on only in one of these models. According to the present knowledge of the pulmonary circulation hemodynamics, an improved definition for the PVR could be obtained: 1. by a multipoint pulmonary vascular pressure/flow plot at high flows and 2. with the use of the pulmonary artery occlusion pressure [PAOP] in addition to the determination of the pulmonary wedge pressure technique [PWP], in order to establish the estimated downstream pressure of the pulmonary circulation at zero flow. Therefore, pulmonary hemodynamic determinations of the PVR are better defined with the analysis of the pressure-flow relationships in addition to the information derived from the PAOP/PWP measurements. However, if none of the previous pressure-flow relationships [in order to obtain the slope = PVR at high flows] or the effective downstream pressure measurements [in order to estimate the critical closing pressure at zero flow] are applied for the analysis of the pulmonary circulation, a cautious interpretation of the measured variables [mean pulmonary artery pressure and cardiac output] is preferable to wrong conclusions made from a meaningless variable, the "calculated PVR".

Correlación clínica-hemodinámica de la clasificación de la NYHA4/WHO en enfermos con hipertensión arterial pulmonar idiopática. Sus implicaciones en la clínica, en el tratamiento y en el pronóstico a largo plazo / Clinical-hemodynamic correlation of the NYHA/WHO system in idiopathic pulmonary artery hypertension. Clinical, therapeutic and long-term prognosis implications

BACKGROUND: The most often used functional classification for categorizing the degree of cardiac disability in patients with chronic left ventricular failure is the NYHAN/WHO system. In Idiopathic Pulmonary Arterial Hypertension [I-PAH], this system although used, has not been studied in detail regarding pulmonary hemodynamic parameters association and for long-term prognosis in each of the NYHA/WHO classes. METHODS: We retrospectively, studied the NYHA/ WHO system in 83 I-PAH patients. Patients were separated according to the response in the acute vasodilator trial in responders [n = 30] and nonresponders [n = 53]. RESULTS: Classes I - II did not represent the minority population for I-PAH patients [58/83 = 60%]. Only mean right atrial pressure [mRAP] and mean pulmonary artery pressure [mPAP] were different among the NYHA/WHO functional classes [p < 0.000 and p <0.012; respectively]. I-PAH patients class I have the probability to be a responder 12.6 times more [CI 95.%: 4.59-40.62; p < 0.000]. The long-term mortality for class I patients was 0.%, for class II: 2.%, for class III: 28.% and for class IV: 63.% [p < 0.0001]. The follow-up change for one grade class of the NYHA/WHO classes at four years was noticed only in 20.% of the I-PAH patients. CONCLUSIONS: NYHA/WHO classes I-II did not represent the minority of I-PAH patients population as has been previously considered. Only mRAP and mPAP were different among the NYHA/WHO classes. The NYHA/ WHO system on the basis of mRAP and mPAP allows to separate classes I-II from III-IV. I-PAH patients class I have 12.6 times more the probability to be a responder and better long-term survival; irrespective of the treatment the prognosis seems to be excellent for this functional class group patients.

La resistencia vascular pulmonar calculada. Un parámetro incierto para la valoración de lacirculación pulmonar. Los métodos actuales para determinarla / Calculated pulmonary vascular resistance, is definitively a worthless variable. Current methods for a better definition

The term pulmonary vascular resistance [PVR] describes, in part, the forces opposing the flow across the pulmonary vascular bed. The equation traditionally used is based on the assumption that the pulmonary capillaries, as well as some others vessels in series behave like a Poiseuille resistance. This assumption implies a laminar type of flow of a homogeneous Newtonian fluid, however blood is not a Newtonian fluid and flow is pulsatile in the pulmonary circulation. Neglecting these factors [which only slightly undermines the application of the equation] and others as well [like distension and recruitment of the vessels], will, however, not give us a true clinically practical solution for the calculation of PVR, because the concept of the equation is only true or partially true for part of the pulmonary circulation. In other parts of the lung, flow depends mainly on the behaviour of capillaries as a Starling resistor. If we considered always pulmonary venous pressure [measured clinically as left atrial pressure or pulmonary wedge pressure] as the effective downstream pressure for the calculation of PVR and we ignore or disregard the existence of a significant [quot ]critical closing pressure[quot ] [whatever the cause] in the lung it will lead to additional erroneous concept regarding PVR calculations and, in addition for the real hemodynamic conditions of the pulmonary vascular bed. Because, at least two different models of perfusion exist in the lung it is inadmissible from a theoretical point of view to calculate PVR, based on only in one of these models. According to the present knowledge of the pulmonary circulation hemodynamics, an improved definition for the PVR could be obtained: 1. by a multipoint pulmonary vascular pressure/flow plot at high flows and 2. with the use of the pulmonary artery occlusion pressure [PAOP] in addition to the determination of the pulmonary wedge pressure technique [PWP], in order to establish the estimated downstream pressure of the pulmonary circulation at zero flow. Therefore, pulmonary hemodynamic determinations of the PVR are better defined with the analysis of the pressure-flow relationships in addition to the information derived from the PAOP/PWP measurements. However, if none of the previous pressure-flow relationships [in order to obtain the slope = PVR at high flows] or the effective downstream pressure measurements [in order to estimate the critical closing pressure at zero flow] are applied for the analy.

[The possible clinical role of the cardiac pulmonary power in patients with primary pulmonary hypertension. Initial observations]. / El análisis del poder cardíaco "pulmonar" en hipertensión arterial pulmonar primaria y secundaria. Observaciones iniciales, su posible utilidad en la clínica.

The heart is a muscular mechanical pump with an ability to generate both flow [cardiac output] and pressure in the systemic circulation as well in the pulmonary vascular bed. The product of flow output and systemic arterial pressure is the rate of useful work done, or cardiac power output [CP], therefore for the right ventricle and the pulmonary arterial vascular bed it will be: the product of flow output and mean pulmonary arterial pressure will be the rate of useful work done, or cardiac pulmonary power output [CPP]. Cardiac pulmonary pumping reserve capability can be defined as the maximal cardiac pulmonary power output [CPP] achieved by the right heart during maximal stimulation. Therefore, CPP reserve is the increase in power output as the cardiac performance is increased from the resting to the maximally stimulated state. Recently, several studies have shown that CP is a direct indicator of overall cardiac function, as well is an indicator of exercise capacity and a powerful predictor of prognosis for patients with severe heart failure and ischemic cardiogenic shock. On this basis: 1. we decided to investigate the possible previously mentioned roles of the CP and CPP in patients with different degrees of pulmonary arterial hypertension [n = 137], but mainly in those with primary pulmonary arterial hypertension [PPH]. PPH patients [n = 50], as well as those with Eisenmenger's syndrome [n = 10] were found to have most abnormal resting CPP Indexes [I], [0.431 +/- 0.171, 0.607 +/- 0.124 watts/m2, respectively]. During exercise in PPH patients [n = 14], both CPI and CPPI reserves although they increase, were also found to be significantly diminished [CPI: from 0.546 +/- 170 to 1,116 +/- 0.275 watts/m2, p < 0.05], [CPPI: from 0.373 +/- 0.156 to 0.837 +/- 0.226 watts/m2, p < 0.05]. 2. We also found, significant differences in resting CPPI between PPH responders and no responders patients to hydralazine [0.273 +/- 0.04, 0.507 +/- 0.142 watts/m2, respectively, p < 0.01]. During exercise and under the influence of hydralazine, CPPI "reserve" was significantly diminished in those patients considered as not responders [0.507 +/- 0.142 to 0.723 +/- 0.232 watts/m2, p = ns] when compared with responders to the vasodilator therapy [0.273 +/- 0.04 to 0.903 +/- 0.057 watts/m2, p < 0.01]. On the basis of these initial findings on CPPI in PPH patients, we think that the values of this parameter should be investigated as an index for classifying the severity of this arterial vascular disease, for selecting patients as responders or not to vasodilator therapy, and in the future, to explore the possibility of is usefulness as a prognostic predictor index of mortality in a large population of patients with PPH.

El análisis del poder cardíaco [quot ]pulmonar[quot ] en hipertensión arterial pulmonar primaria y secundaria. Observaciones iniciales, su posible utilidad en la clínica / The possible clinical role of the cardiac pulmonary power in patients with primary pulmonary hypertension. Initial observations

The heart is a muscular mechanical pump with an ability to generate both flow [cardiac output] and pressure in the systemic circulation as well in the pulmonary vascular bed. The product of flow output and systemic arterial pressure is the rate of useful work done, or cardiac power output [CP], therefore for the right ventricle and the pulmonary arterial vascular bed it will be: the product of flow output and mean pulmonary arterial pressure will be the rate of useful work done, or cardiac pulmonary power output [CPP]. Cardiac pulmonary pumping reserve capability can be defined as the maximal cardiac pulmonary power output [CPP] achieved by the right heart during maximal stimulation. Therefore, CPP reserve is the increase in power output as the cardiac performance is increased from the resting to the maximally stimulated state. Recently, several studies have shown that CP is a direct indicator of overall cardiac function, as well is an indicator of exercise capacity and a powerful predictor of prognosis for patients with severe heart failure and ischemic cardiogenic shock. On this basis: 1. we decided to investigate the possible previously mentioned roles of the CP and CPP in patients with different degrees of pulmonary arterial hypertension [n = 137], but mainly in those with primary pulmonary arterial hypertension [PPH]. PPH patients [n = 50], as well as those with Eisenmenger's syndrome [n = 10] were found to have most abnormal resting CPP Indexes [I], [0.431 +/- 0.171, 0.607 +/- 0.124 watts/m2, respectively]. During exercise in PPH patients [n = 14], both CPI and CPPI reserves although they increase, were also found to be significantly diminished [CPI: from 0.546 +/- 170 to 1,116 +/- 0.275 watts/m2, p < 0.05], [CPPI: from 0.373 +/- 0.156 to 0.837 +/- 0.226 watts/m2, p < 0.05]. 2. We also found, significant differences in resting CPPI between PPH responders and no responders patients to hydralazine [0.273 +/- 0.04, 0.507 +/- 0.142 watts/m2, respectively, p < 0.01]. During exercise and under the influence of hydralazine, CPPI [quot ]reserve[quot ] was significantly diminished in those patients considered as not responders [0.507 +/- 0.142 to 0.723 +/- 0.232 watts/m2, p = ns] when compared with responders to the vasodilator therapy [0.273 +/- 0.04 to 0.903 +/- 0.057 watts/m2, p < 0.01]. On the basis of these initial findings on CPPI in PPH patients, we think that the values of this parameter should be investigated as an index for classifying the se...

Disminución de hemorragias totales con dosis reducidas de enoxaparina en angina inestable de alto riesgo / Estudio ENHNFAI. (ENoxaparina vs Heparina No Fraccionada en Angina inestable). Informe preliminar. Decrease of total hemorrhage with reduced doses of enoxaparin in high risk unstable angina. ENHNFAI study. (Enoxaparin vs non-fractionated heparin in unstable angina). Preliminary report

In this prospective, randomized and controlled study, we compare complications in 2 groups of patients: group 1, enoxaparin 0.8 mg/kg, subcutaneous every 12 hours during 5 days, and group 2, intravenous unfractionated heparin during 5 days, by infusion treated to activate partial tromboplastin time 1.5-2 the upper limit of normal. Blood samples were obtained at 4, 12, 24 hours and at day 5 of treatment, to measure anti-Xa levels, and also, evaluated end points at 30 days, between groups. Univariate and multivariate logistic regression analyses were performed with clinical and angiographic variables between groups, with p < 0.05. RESULTS: 203 consecutive patients, average age of 60.5 +/- 11.2 years, and 80 men, were included. There were no differences in clinical and angiographic characteristics. All patients with enoxaparin had therapeutic levels of anti-Xa, of 0.5 to 0.67 U/mL. There was increasing risk of total bleeding in group 2 (18.7) than in group 1 (5.6), with RR = 1.72 (95 CI 1.29, 2.29), p = .003. Also, there was 33.3 of MACE in group 2, and only 17.8 in group 1, with RR = 1.88 (CI 95 1.29, 2.29), p = .011. CONCLUSIONS: 1) Low doses of enoxaparine achieve therapeutic levels, since the first 4 hours of treatment. 2) A significant reduction of total bleeding occurred with the low doses of enoxaparin, with the same efficacy to reduce MACE during follow-up.