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Eulo Lupi Herrera

Publications and source records attributed to Eulo Lupi Herrera.

9 recordsLinked to original sources
PubMedDate not supplied

[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].

UNLABELLED: 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.

Aged↗
PubMedDate not supplied

[National Registry of Acute Ischemic Coronary Syndromes (RENASICA). Mexican Cardiology Society. The RENASICA Cooperative Group].

This study assessed current practices in relation to coronary risk factors, therapy and its results in patients with acute ischemic coronary syndromes (AICS) with or without ST-segment-elevation myocardial infarction [MI], from data collected in the National Registry of AICS [RENASICA] in México; Eigh teen hospitals [2nd. and 3rd level of medical attention] recruited patients for the registry, 4,253 patients were enrolled, 2,773 [65.2%] without AICSST segment elevation and 1480 [34.8%] patients with ST segment elevation MI. Chest pain was the main cause for seeking medical attention to an emergency service (90.5%) and 50% of the patients referred it in advance. AICS was mainly observed in men in their sixth decade of age. Age, ST segment depression [> 2 mm], CKMB [> 2 values above normal] and the extension of the coronary artery disease allow to predict mortality and the combination of mortality and myocardial infarction. Only 50.4% of the eligible patients with AICS and ST-segment-elevation myocardial infarction received thrombolytic therapy. Of the eligible cohort of AICS only 58% patients could an hemodynamic study be performed. In 55% of them, a percutaneous coronary intervention procedure was done (PTCA-Stent implantation). Aspirin [ASA] and heparin were prescribed in 70% of the patients at entry to the ward and the same percentage of AICS patients received ASA after discharge. Low molecular weight heparin and IIb/IIIa receptor platelet antagonists were used in a low proportion of patients. RENASICA provides information related to AICS patients that could help the mexican health authorities to apply better the health resources in the forthcoming future for the treatment of AICS.

Adolescent↗
PubMedDate not supplied

["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, "or the cardiac power" (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.

Cardiac Output↗
PubMedDate not supplied

[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.

Angioplasty, Balloon, Coronary↗
PubMedDate not supplied

[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 "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.

Blood Pressure↗
PubMedDate not supplied

[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.

Acute Disease↗
PubMedDate not supplied

[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 "Cardiac power" that is the product of flow and arterial pressure and that is of utility to know the "Miocardial reserve". In our experience after reperfusion procedure patients with CHC and cardiac power less than 1.0 had highly mortality.

Cardiac Output↗