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A Bayés de Luna

Publications and source records attributed to A Bayés de Luna.

At least 19 recordsLinked to original sources
PubMed2002

Sustained ventricular tachycardia as a marker of inadequate myocardial perfusion during the acute phase of myocardial infarction.

BACKGROUND: Sustained ventricular tachycardia (VT) complicating the acute phase of myocardial infarction (AMI) is a quite rare event but with short-term unfavorable prognosis. The clinical characteristics as well as the therapeutic implications have not yet been well defined. HYPOTHESIS: This paper attempts to prove that VT may be considered a marker of inadequate myocardial perfusion after thrombolysis. METHODS: To assess the clinic-electroangiographic characteristics and prognosis of patients with VT occurring within the first 4 days of an AMI, a case-control study was carried out in 23 patients from a total of 1,100 patients (1.9%) hospitalized with AMI between March 1993 and July 1997. These patients were compared with a control group of 131 patients hospitalized consecutively. A statistical analysis was made using the chi-square test, t-test, and logistic regression. RESULTS: There were no differences among groups with regard to age, gender, and area of necrosis. Average time for the onset of VT was 26 h (range 0-92 h). Sixteen patients underwent coronary angiography: 4 patients had left main coronary artery disease, 2 had single-vessel disease, 8 had lesions in two vessels, and 2 had triple-vessel disease. Univariate analysis showed that patients with VT had a higher incidence of creatine phosphokinase (CPK)-MB peak > 300 UI/l (61 vs. 30%; p<0.001), more frequent occurrence of previous AMI (48 vs. 17%; p<0.001), and acute intraventricular conduction disorders (26 vs. 4%; p<0.001). Furthermore, these patients suffered ischemia previous to VT more frequently (65 vs. 11%; p<0.0001), and had a greater mortality rate than that in the control group (35 vs. 4%; p<0.0001). In the multivariant analysis, the variables related to the occurrence of VT were CPK-MB peak > 300 IU/l (OR 5.9; 95% CI 1.6-21), acute intraventricular conduction disorders (OR 9.02; 95% CI 1.7-48), and ischemia immediately prior to VT (odds ratio [OR] 19.64; 95% confidence interval [CI] 5.3-73). CONCLUSIONS: Ventricular tachycardia may be considered a marker of inadequate myocardial perfusion after thrombolysis; therefore, a more aggressive revascularization treatment in these patients would be advisable. The profile of patients with AMI, hospitalized in the coronary care unit, who will likely suffer from VT is previous AMI, CPK-MB peak > 300, acute intraventricular conduction disorders, Killip > I, and ischemia previous to VT.

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PubMed1999

Elevated levels of plasmin-alpha2 antiplasmin complexes in unstable angina.

The evidence of elevated levels of several biochemical markers of prothrombotic state in patients with unstable angina suggests that thrombus formation and lysis play a pivotal role in acute coronary syndromes. The clinical syndrome of unstable angina encompasses a variety of clinical presentations of transient episodes of myocardial ischemia. This study was designed to assess plasmin generation in different settings of unstable angina. Evidence of plasmin generation in patients with unstable angina was measured by circulating plasmin-alpha2 antiplasmin complexes (PAP). A second objective was to identify whether PAP levels had a prognostic value to predict outcome. Eighty-five patients admitted to the coronary care unit for unstable angina were classified into three groups. Group A included 26 patients with postinfarction angina; group B comprised 26 patients with new onset angina; and group C included 33 patients with crescendo angina. Mean PAP levels were higher in the three groups compared to healthy controls. A significant correlation was found between levels of PAP and D-dimer, particularly in postinfarction angina (r = 0.6; p <0.0005). This trial adds new insights into the pathophysiology of unstable angina. It demonstrates that plasmin is generated in the different settings of unstable angina but particularly in postinfarction angina patients where a fibrin-rich thrombus is responsible of the symptoms. However, in this series PAP levels do not predict an uneventful outcome neither in the acute phase nor at long term (6 months).

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PubMed1997

Comparison of morphologic assessment of hypertrophic cardiomyopathy by magnetic resonance versus echocardiographic imaging.

To compare the value of echocardiography and magnetic resonance imaging (MRI) in the assessment of the amount and extent of hypertrophy in hypertrophic cardiomyopathy (HC) and, second, to correlate the degree of hypertrophy, as assessed by MRI, with clinical and electrocardiographic parameters, 30 consecutive patients (16 men and 14 women, aged 20 to 74 years) with HC were studied. Measurements of left ventricular wall thickness were performed at 11 predetermined segments (5 basal, 5 midventricular, and 1 apical) by 2-dimensional echocardiography and MRI. Two parameters derived from MRI studies were considered as indicators of the degree and extent of hypertrophy: (1) mean of the measured wall thickness at the 11 segments, and (2) the number of segments with thickness > 15 mm. Results showed that, from a total of 330 myocardial segments, thickness could be measured by echocardiography in 221 (67%), whereas MRI allowed measurement of 320 segments (97%). When compared with clinical and electrocardiographic data, no correlation was found regarding mean wall thickness and number of hypertrophied segments by MRI except for the presence of an abnormal electrocardiographic repolarization pattern. It is concluded that MRI allows a better assessment of the degree and extension of left ventricular hypertrophy than echocardiography in HC. Despite the precise information on hypertrophy provided by MRI, the amount and degree of hypertrophy bears no correlation with most of the clinical data in these patients.

Adult↗
PubMed1997

Automatic measurement of corrected QT interval in Holter recordings: comparison of its dynamic behavior in patients after myocardial infarction with and without life-threatening arrhythmias.

This study was designed to determine the value of automatic corrected QT-interval measurement in Holter tapes in patients after myocardial infarction as a marker of life-threatening ventricular arrhythmias. We compared the corrected QT interval, automatically measured in 24-hour Holter recordings, in two groups of patients after myocardial infarction: group I was composed of 14 patients admitted consecutively to our hospital for documented sustained ventricular tachycardia or out-of-hospital cardiac arrest. Group II consisted of 28 patients with previous myocardial infarction with characteristics similar to those of group I, but without malignant ventricular arrhythmias in the follow-up. The global mean 24-hour corrected QT interval was longer in group I (425 +/- 20 msec) than in those patients after myocardial infarction without arrhythmias (group II) (405 +/- 17 msec; p < 0.01). Furthermore, a significant proportion of patients of group I (seven of 14) exhibited more peaks of corrected QT longer than 500 msec compared with patients of group II (two of 28; p < 0.005). A circadian rhythm of corrected QT peaks was observed in group I, having a significantly higher incidence from 11 PM to 11 AM (p < 0.05). We conclude that automatic corrected QT-interval measurement on Holter electrocardiogram is now available and feasible. Our results suggest that this is a marker for risk assessment of life-threatening ventricular arrhythmias. Large-scale trials are needed to confirm these results and to determine the predictive value of this technique for risk stratification.

Algorithms↗
PubMed1996

[Sudden death in heart failure].

INTRODUCTION: Our study was designed with the primary objective of evaluating the cardiac, overall and sudden mortality in patients with class IV heart failure (NYHA) managed with standard treatment and captopril (50 mg/8 hr. max.). MATERIAL AND METHODS: 95 consecutive patients were enrolled in 21 hospitals and were followed for 6 months in order to design an interventional clinical trial to reduce sudden death. RESULTS: Death occurred in 14 patients (14.7%; i.c. 8.3% - 23.5%; p < 0.05). There were no non-cardiovascular deaths in the group. There were 6 sudden death cases (42.9%; i.c. 16.9% - 68.8%, p < 0.05). Patients who died had a higher baseline end-diastolic (p < 0.05) and end-systolic (p < 0.01) diameter of the left ventricle (LV) and lower values of systolic (p < 0.01) and diastolic (p < 0.05) blood pressure. During the follow-up phase, heart rate, ventricular premature contraction, blood pressure and LV diameters decreased significantly in the whole group (p < 0.05, p < 0.001). We found no any differences during the follow-up phase between the patients who died and those who survived. In the patients who died we found no any differences between sudden death cases and the other death cases. CONCLUSIONS: Sudden death was less frequent than we had expected and due to this fact it is impossible for us to design an interventional trial.

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