ABSTRACT
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...
Subject(s)
Female , Humans , Male , Blood Pressure , Cardiac Output , Hypertension, Pulmonary , Exercise TestABSTRACT
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.