Objective: There is considerable knowledge of the incidence of torsades de pointes (TdP) during the administration of amiodarone The aim of our study was to determine the incidence of TdP during the loading phase of intravenous administration of amiodarone, intended to reverse paroxysmal atrial fibrillation (PAF) to sinus rhythm (SR), and to test the hypothesis that their prevalence is greater among women than men, as reported earlier. We also sought to determine factors predisposing to the occurrence of TpD, such as atrium size and hyperglycemia. Methods: We evaluated 189 patients (M = 107, F = 82, mean age = 56 ± 19 years), who were admitted for PAF, and for whom amiodarone was selected as the first-choice drug for PAF reversion. During the first 24 h of the loading phase (300 mg rapid i.v. administration within 20 min and 1,500 mg i.v. for 24 h) we recorded all ventricular arrhythmias. All patients were on anticoagulant treatment and all of them were evaluated for corrected QT (QTc), as well as additional risk factors (atrial size, serum glucose, hypopotassemia, hypomagnesemia, severe bradycardia). Patients with heart failure, hypertrophic obstructive cardiomyopathy, a history of coronary artery disease or ventricular tachycardia, as well as those treated with drugs prolonging the QT interval, were excluded from the study. Results: 108 patients (57.1%) experienced successful conversion of PAF into SR on amiodarone. Five patients (2.6%), all female, mean age 53.0 ± 1.2 years, developed TpD. All episodes occurred at the end of the loading phase (21–24 h) of amiodarone administration. None of them had hypopotassemia, hypomagnesemia, or bradycardia (HR <55 bpm). Two of the TpD patients had elevated glucose levels, and all of them had prolonged QTc immediately prior to the TpD. Conclusion: We confirm that women are at increased risk of developing TpD during the administration of amiodarone. TpD develop towards the end of the intravenous loading phase; the electrocardiographic changes should be closely monitored towards the end of the loading phase. The presence of diabetes mellitus or temporal hyperglycemia and prolonged QTc seems to be predicting factors for TpD during i.v. amiodarone administration.
There is a growing interest in immunologically-mediated lesions in the cardiovascular system, as there has been evidence that there are antimitochondrial antibodies (AMA) in patients with hypertrophic cardiomyopathy or hypertensives with left ventricular hypertrophy (LVH). We have also very recently published findings from our laboratory that hypertensives with LVH have a considerable quantity of anticardiac antibodies (ACA) in their serum. The aim of this study was to investigate the possible involvement of autoimmune mechanisms in the pathogenesis and evolution of hypertensive disease. Three groups of subjects were included in the study. Group A comprised 37 patients (20 men, 17 women, mean age 50.5 +/- 8.5 years) with mild to moderate essential hypertension, 19 without echocardiographic evidence of LVH, and 18 with LVH. Group B comprised 10 patients (6 men, 4 women, mean age 45.1 +/- 8.7 years) with secondary hypertension. The control group (C) comprised 15 normotensive subjects (8 men, 7 women, mean age 47.7 +/- 8.7 years). Cellular immunity against arterial wall antigen was studied in all subjects by means of migration inhibitory factor (MIF) against relevant antigen preparation. Sera from Group A and C subjects were tested for the presence of autoantibodies against both specific (myocardial) and nonspecific antigens, by means of the indirect immunofluorescence technique. Eighty per cent of patients with essential hypertension showed a positive cellular response (MIF) against an arterial wall antigen compared to the patients with secondary hypertension or the control group. Moreover, patients with essential hypertension and LVH had the highest incidence of specific (anticardiac, ACA) and nonspecific autoantibodies and the highest C3c and C4 complement component levels compared to patients without LVH or the control group. Most of the ACA positive patients were also AMA positive, while the ACA negative patients were AMA negative as well. Defects in cell-mediated immunity against arterial wall antigen(s) may be the cause or the effect of hypertension. On the basis of our findings that there was no delayed type hypersensitivity response to arterial wall antigen(s) in the patients with secondary hypertension, we suggest that, in some cases of essential hypertension, delayed hypersensitivity reactions possibly contribute to the pathogenesis of hypertension. Autoimmune mechanisms are discussed on the basis of common epitopes shared between heart and arterial tissue.
The purpose of the study was to investigate the possible role of autoantibodies in the development and type of left-ventricular hypertrophy (LVH). Three groups of subjects were studied:15 patients with hypertrophic cardiomyopathy (HCM; 11 males, 4 females; mean age 50.0 ± 16..3 years); (b) 15 patients with essential hypertension (10 males, 5 females; mean age 56.8 ± 13.5 years) with normal renal function and serum electrolytes and (c) 15 male athletes (mean age 20.8 ± 5.9 years). The control group consisted of 15 normal subjects with no sign of heart disease. The following indices of cardiac performance were determined by means of echocardiography: end-diastolic and end-systolic diameters, interventricular septum thickness, left-ventricular (LV) wall thickness, LV mass and LV mass index. The immunologic parameters studied included autoantibodies against (a) specific (anticardiac cell; ACA) and nonspecific (antimitochondrial cell; AMA) autoantigens according to a conventional indirect immunofluorescence technique. (1) Higher values for LV mass and LV mass index were observed in HCM. (2) The incidence of specific and nonspecific autoantibodies in hypertensive patients and in patients with HCM was significantly higher compared to athletes and controls. All ACA-positive individuals (5 with HCM, 3 with hypertension and 1 athlete) were AMA positive as well, while all ACA-negative individuals were also AMA negative. The ACA-positive individuals had higher C3c and C4 levels compared to the ACA-negative individuals. An autoantibody-mediated immunopathogenic role is discussed in the development and type of myocardial hypertrophy. Left-ventricular hypertrophy (LVH) due to heart disease (cardiomyopathies, hypertension or aortic stenosis) is considered as a pathological process followed by fibrosis and structural muscle changes [1]. On the contrary, LVH in athletes is considered as a ‘physiological’ myocardial response to exercise [2]. On the other hand, Autore et al. [3] have reported the presence of autoantibodies against mitochondria in patients with cardiomyopathies or hypertension with LVH, but not in athletes with LVH. These findings suggest the possibility that autoimmune mechanisms might be involved in the pathogenesis of LVH due to heart disease In this study we sought for the presence of autoantibodies against both specific and nonspecific antigens in athletes and patients with LVH of different origins, such as hypertrophic cardiomyopathy (HCM) or hypertension, in order to investigate the possible involvement of these autoantibodies in the development of LVH.
The prevalence and severity of coronary atherosclerosis increase dramatically with age, so that more than half of all deaths in persons aged over 65 are due to coronary arterial disease (CAD) and about three fourths of all deaths from CAD occur in the elderly. The aims of our study were, first, to detect myocardial ischemia development in elderly versus younger patients undergoing treatment for known CAD through the use of both conventional treadmill testing and 201T1 scintigraphy, and second, to determine the relationship between the above non-invasive tests and angiographically confirmed important coronary artery disease (iCAD). A database of 606 patients (355 men and 251 women) who had undergone coronary angiography, exercise ECG testing (ETT) using the treadmill Bruce protocol, and 201T1 scintigraphy, was reviewed retrospectively. All patients had displayed clinical expression of CAD with or without the existence of an old myocardial infarction (MI). The patients were from both sexes (440 men and 252 women) and divided into two groups, according to age. Group A was composed of 265 patients aged over 65 (170 men, 95 women, mean age = 70.3 +/- 5.3 years). Group B was composed of 341 patients aged under 65 (185 men, 156 women, mean age 54.4 +/- 9.1 years). Patients with uncontrolled arterial hypertension, hypertrophic cardiomyopathy, severe valve diseases, severe chronic obstructive lung diseases, severe anemia, peripheral atherosclerosis, orthopedic problems, or Parkinson's disease were excluded from the study. The term "important coronary artery disease" (iCAD) covers the following patterns of coronary anatomy: (a) left main stem stenosis > or = 50% with or without disease elsewhere, (b) proximal three-vessel disease, (c) three-vessel disease including the proximal left anterior descending artery (LAD), (d) proximal two-vessel disease including LAD, and (e) two-vessel disease including the proximal LAD. Biostatistical characteristics such as sensitivity, specificity, and predictive values of ETT-201T1 were estimated. Analyzing our results we concluded that: the biostatistical parameters in predicting important CAD in elderly and younger patients by means of exercise test and thallium scintigraphy need to be redefined through more closely scheduled and prospective studies; in elderly coronary patients, the appearance of positive results in both parameters of ETT-201T1 indicates a significant possibility of iCAD existence; in coronary patients younger than 65 years, the appearance of negative results in both parameters of ETT-201T1 almost excludes iCAD, in contrast to elderly patients, who display a significant proportion of iCAD; in elderly coronary patients, the appearance of equivocal results in both tests indicates a significant possibility of the existence of iCAD, in contrast to younger patients.
The study describes the changes in basic hemodynamic parameters after long-term antihypertensive therapy with cilazapril - a new ACE inhibitor lacking a sulfhydryl group - in hypertensive patients and the drug effects on renal function, glucose tolerance and lipid metabolism. 30 patients (18 males, 12 females, mean age: 53.3 ± 18 years) with mild to moderate essential hypertension were studied. The following determinations were performed in patients, before and after 4.5 months of cilazapril monotherapy at a dose of 5 mg/24 h: (a) antihypertensive action of the drug (arterial pressure at rest and during a 24-hour recording); drug effects on left ventricular (LV) mass index; its contractility indexes (%FS, EF) and the left atrial emptying index were studied by means of echocardiography; plasma insulin concentration during oral glucose tolerance tests, in the fasting state, after the administration of 75 g glucose per os, as well as the changes in the insulinogenic index and the 6-keto-PGF1α/TXB2 ratio, and drug effect on renal function (urea, creatinine, uric acid, plasma electrolytes), blood lipid profile (total cholesterol, triglycerides, HDL-CH) and serum transaminases. Long-term drug administration exhibits an effective antihypertensive action, without causing reflex tachycardia and also reduces the LV mass index without affecting its EF, while improving its diastolic function. It does not significantly affect the various biochemical parameters, and achieves glucose regulation, both in the fasting state and after glucose loading, with a decrease in the insulinogenic index, and simultaneously increases the 6-keto-PGF1α/TXB2 ratio. The existence of a direct cause-effect relationship between the changes in the above hormone systems is possible.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.