[Oral Verapamil therapy in cardiac arrhythmias].
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Keywords:
Cardiac arrhythmia
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Dilated Cardiomyopathy
Doppler imaging
Diastolic heart failure
Brain natriuretic peptide
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The current study was performed in order to investigate whether verapamil would affect the glucose response to glucagon differently in patients with non insulin-dependent diabetes mellitus (NIDDM) compared with age-matched normoglycemic controls. For that purpose glucagon was injected intravenously on a background infusion of verapamil, and for comparison also on a background infusion of saline in these two groups. Verapamil was found to blunt the glucose response to glucagon in the patients with NIDDM, whereas it augmented the glucose response to glucagon in the controls. This discrepancy could not be explained on the basis of verapamil-induced changes in the release of insulin, since verapamil did not effect the serum responses to glucagon. However, it could reflect the differences in hepatic handling of glucose, which has been shown to prevail in patients with NIDDM compared with healthy controls.
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Left atrial enlargement
Univariate analysis
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Effects of Verapamil on Diurnal and Thyrotropin-Releasing Hormone-Stimulated Prolactin Levels in Man
The effects of the calcium entry blocker vera-pamil on the 24-h profile of PRL secretion and on the PRL response to TRH were investigated in six healthy volunteers. Verapamil (120 mg, three times daily) was administered orally for 1 week. In all subjects both basal and TRH-stimulated PRL levels were markedly elevated by verapamil. The average diurnal PRL concentration was increased from 13.0 ± 2.0 μg/L to 25.2 ± 4.4 (mean ± se; P = 0.02). Diurnal rhythm and pulsatility of PRL secretion were seen both before and during verapamil administration. Mean peak PRL concentrations after TRH injection (200 μg, iv) were significantly increased from 72.6 ± 11.6 t o 115.2 ± 16.8 (P < 0.01), and the mean area under the PRL concentration-time curves from 4332 ± 962 μg/L·120 min to 6975 ± 1334 (P = 0.01). The data are in striking contrast with previous findings from in vitro studies where verapamil has been reported to block calcium-mediated stimulus-secretion coupling and inhibit hormone secretion from pituitary cells. Interference with other PRL-regulating mechanisms may account for the demonstrated verapamil-induced PRL secretion in vivo.
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Purpose: We aimed to investigate if baseline NTproBNP and clinical variables, predict incident atrial fibrillation (AF) in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI). Methods: From a prospective registry, we assessed 984 PPCI patients. In univariate and multivariate regression analysis, we investigated the association of NTproBNP level determined just prior to PPCI, peri-procedural systolic and diastolic blood pressure, infarct size (maximum CK), gender and age, with the incidence of AF. A Kaplan-Meier curve with quartiles of NTproBNP was computed with a log-rank test to assess for significance of differences. Results: NTproBNP was higher (1297 pg/ml versus 570 pg/ml) in patients with versus without incident AF. In univariate analysis, NTproBNP was significantly associated with incident AF (OR 1,11, 95% CI 1,03-1,21, P=0,009). In multivariate analysis, age was the strongest predictor of incident AF (highest quartiles versus lowest quartile OR 7,04, 95% CI 2,77 -17,87, P<0,001). NTproBNP (OR 1,09, 95% CI 1,00 -1,20, P=0,049), systolic blood pressure (OR 0,98, 95% CI 0,97 -1,00, P=0,021) and infarct size (OR 1,18, 95% CI 1,04 -1,33, P=0,01) were also independently associated with incident AF. Gender, target lesion vessel and diastolic blood pressure were not associated with incident AF. Kaplan-Meier curves (Figure 1) depict that higher NTproBNP quartile is significantly (P=0,001) associated with incident AF. Figure 1. Kaplan-Meier curves Conclusion: Age is strongly predictive for incident AF in STEMI patients undergoing PPCI. NTproBNP and infarct size are also independent predictors of incident AF, whereas peri-procedural systolic blood pressure is inversely related to incident AF.
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Left ventricular remodeling (LVR), an increase in left ventricular end-diastolic volume index > or = 20%, is an adverse consequence of myocardial infarction. The aim of this study was to assess the association between LVR and adiponectin, which has been shown to protect against myocardial ischemia-reperfusion injury.In 75 patients echocardiographic examination was performed one year after ST-segment elevation myocardial infarction, successfully treated with primary percutaneous coronary intervention (pPCI). Two groups of patients were analyzed: those with LVR (n = 15) and those without LVR (n = 60).The predictors of LVR were: anterior myocardial infarction, glucose at admission, baseline C-reactive protein, adiponectin, and echocardiographic parameters: left ventricular end-diastolic and end-systolic volume indices, ejection fraction < 40% and left ventricular wall motion score index (WMSI) at discharge. On multivariable regression analysis, lower adiponectin level (OR = 0.67, 95% CI 0.49-0.91, p < 0.05) and higher WMSI (OR = 20.14, 95% CI 2.62-154.82, p < 0.01) were the only independent negative predictors of LVR. The optimal cut-off for adiponectin for predicting LVR was < or = 4.7 mg/mL (sensitivity: 73%, specificity: 85%) and this level increased the risk of LVR 15-fold (95% CI 4.05-59.87, p = 0.0001).Baseline low blood adiponectin concentration, along with WMSI, can be considered as a predictor of the LVR in male patients one year after myocardial infarction and pPCI.
Ventricular remodeling
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It is known that not only postinfarction left ventricular (LV) remodeling but also chronic regional myocardial hypoperfusion may cause a compensatory hypertrophy of undamaged areas of the left ventricle. Can chronic LV hypoperfusion lead to the development of mitral regurgitation (MR) in CAD patients without previous myocardial infarction We selected patients with significant coronary stenosis (>75%) of at least one epicardial artery who had no acute or previous myocardial infarction: 1162 patients without MR and 76 patients with moderate and severe MR. Patients with MR more often had higher NYHA functional class (II-IV) (91.7 vs 63.0%, p =0.004) and arrhythmias (60.3 vs 14.6%, p<0.001). They also had significantly higher echocardiographic indices of left atrial dimension (23.5+/-2.9 vs. 20.3+/-2.1 mm/m2). MR was independently associated with NYHA class of congestive heart failure, arrhythmias, and index of the left atrium size. No association between MR and the localization of significant coronary lesions was found.
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This study was performed to determine the relation between inducible sustained ventricular tachycardia (ISVT) by programmed electrical stimulation and angiographic, clinical and echographic data in patients with coronary artery disease. The aim of this study was to explore if these inducible arrhythmias are associated with any specific "arrhythmogenic" pattern of coronary artery disease. 129 consecutive patients with coronary artery disease and ISVT were evaluated by left ventriculography and coronary arteriography by standard techniques. The mean age of the patients was 46 years with a range of 21 to 72 years, 74% of them were males. A significant stenosis of the main left coronary artery (>50%) appeared to be more frequent in arrhythmia patients (31%). Also proximal left anterior descending artery stenosis was more frequent in in the arrhythmia patients (48%). "Main left equivalent" lesions, defined as a significant stenosis of the proximal left anterior descending artery and the proximal left circumflex artery was significantly more frequent among the arrhythmia patients (51%). Using the quantitive wall motion analysis, a strong relationship was found between the number of abnormally contracting segments and the presence of inducible sustained ventricular tachycardia. The results of the present study suggest that ISVT in patients with coronary artery disease are more frequently associated with lesions of the main left coronary artery or the proximal left anterior descending artery.
Circumflex
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Paroxysmal atrial fibrillation
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