[When should heart failure be treated with anti-arrhythmia agents? Can the prognosis be improved?].
Explore the source record for details and available documents.
Anti-Arrhythmia Agents↗
Biomedical subjects
T Meinertz
Publications and source records attributed to T Meinertz.
Incidence and clinical relevance of QT prolongation caused by the new selective serotonin antagonist ketanserin. Multicenter Ketanserin Research Group.
Efficacy and safety of ketanserin was studied prospectively in a randomized and double-blind trial involving 221 patients treated for hypertension and/or coronary artery disease. Since ketanserin has been suggested to cause QTc prolongation, we investigated the incidence and severity of this effect, as well as its influence on the incidence of malignant ventricular arrhythmias during Holter monitoring. After a 1-week run-in-period, all patients were examined, measuring blood pressure, electrocardiogram (ECG) and 24-hour Holter ECG. Two thirds of the patients (n = 147) were then randomized to ketanserin, 1 week 20 mg b.i.d. followed by 3 weeks 40 mg b.i.d.; one third of the patients (n = 74) received placebo b.i.d. for 4 weeks. After 4 weeks of treatment, blood pressure, ECG and 24-hour Holter ECG were performed. In hypertensive patients, ketanserin resulted in a significant reduction of systolic (mean reduction: -17 +/- 2 mm Hg; p less than 0.0001) and diastolic blood pressure (-12 +/- 1 mm Hg; p less than 0.0001) as compared to baseline, and to the placebo group (p less than 0.005 for systolic and diastolic blood pressure). The QTc interval was prolonged with ketanserin (mean value: 400 to 418 ms; p less than 0.01) but not with placebo (399 vs. 402 ms). In the ketanserin group 30% of patients and in the placebo group 8% of patients had QTc prolongation greater than 30 ms (p less than 0.01). QTc was not prolonged to greater than 500 ms in any patient. During Holter monitoring 128/147 patients (ketanserin group) and 61/74 patients (placebo group) had ventricular premature beats; in 42 (ketanserin group) and 13 patients (placebo group) ventricular pairs and tachycardia were documented. Incidence and severity of the ventricular arrhythmias after 4 weeks of treatment were not different between the ketanserin and placebo groups. No sustained ventricular tachycardia occurred in any patient after ketanserin treatment. Thus, though ketanserin prolonged QTc in one third of the patients, the drug was not arrhythmogenic or antiarrhythmic.
Aged↗
[Effect of atrial natriuretic factor on coronary vascular tone].
To test whether atrial natriuretic factor (ANF) may be involved in the modulation of coronary vasomotor tone, ANF was injected into angiographically normal left coronary arteries. Measurement of epicardial diameters of the circumflex (Cx) and left anterior descending artery (LAD) were made from biplane angiograms by an automatic contour-detection system. Bolus injection of ANF (0.07 micrograms/kg, diluted in 1 ml 0.9% NaCl, n = 7) increased diameter of proximal segments of LAD (11 +/- 4%) and Cx (10 +/- 4%) (p less than 0.02 each vs control) without altering heart rate and mean arterial pressure (MAP). Intracoronary nitroglycerin (NTG, 0.3 mg) increased diameters of identical LAD and Cx segments by 18 +/- 3% and 20 +/- 4%. Intracoronary ANF infusion (0.02 micrograms/kg/min over 5 min, followed by 0.1 micrograms/kg/min, n = 10) exerted dose-dependent increases in diameters of LAD and Cx (low dose: + 5 +/- 2%, p less than 0.05 vs control; high dose: + 13 +/- 3%, p less than 0.01 vs control). ANF-infusion increased arterial plasma ANF levels from 280 +/- 80 pg/ml during control to 894 +/- 82 pg/ml (low dose; + 614 pg/ml vs control) and to 2290 +/- 228 pg/ml (high dose). Severe ischemia in four patients undergoing angioplasty exerted substantial increase in arterial ANF levels (160 +/- 60 to 608 +/- 111 pg/ml; + 448 pg/ml vs control), similar to the increase elicited by low dose ANF infusion in man.(ABSTRACT TRUNCATED AT 250 WORDS)
Atrial Natriuretic Factor↗
[How are tachycardic cardiac arrhythmias modified by therapy of congestive heart failure?].
Previous studies have demonstrated the high prevalence of frequent and complex ventricular arrhythmias in patients with severe congestive heart failure. It has been claimed that these arrhythmias are independent risk factors of prognosis. Moreover in severely depressed left ventricular function frequent and repetitive arrhythmias may deteriorate the hemodynamic situation. Recent clinical studies have drawn increasing attention to the possibility that the desired therapeutic effect of Class I antiarrhythmic agents may be complicated by their ability to aggravate the arrhythmia or to provoke new arrhythmias. These "proarrhythmical effects" were more frequent in patients with life-threatening arrhythmias and in those with severely depressed left ventricular function. Prevention trials with Class I antiarrhythmic agents have failed to show beneficial effects on the arrhythmia profile and on the prognosis of those patients. On the other hand, it is now well recognized that the incidence of cardiac death can be reduced by the use of ACE-inhibitors in this patient population. Accordingly, there is evidence of a reduced incidence of complex ventricular arrhythmias during treatment with these drugs in some of the patients with congestive heart failure. The influence of digitalis on the arrhythmia profile and the cardiac mortality in these patients is still a matter of debate. On the other hand, there is evidence that newer positive inotropic agents such as phosphodiesterase-inhibitors rather increase the number of arrhythmias and the prevalence of sudden cardiac death in this patient population.
Angiotensin-Converting Enzyme Inhibitors↗
[Transesophageal echocardiography in the assessment of the severity of aortic valve stenosis].
The aortic valve orifice area was measured in 95 patients with valvular aortic stenosis by means of transthoracic and transesophageal echocardiography. These results were compared to invasively determined measurements. The aortic-valve orifice area could be measured by transesophageal echocardiography in 87 patients (92%), and in 13 patients (14%) by the transthoracic approach. A comparison of the valve-orifice area determined by transthoracic and transesophageal echocardiography revealed a correlation coefficient of r = 0.91. There was also a good agreement when the aortic-valve orifice area determined by transesophageal echocardiography was compared to the invasive findings (r = 0.82; p less than 0.001). The morphology of the aortic valve could be better delineated with the transesophageal approach.
Adult↗
Catecholamine metabolism in patients with congestive heart failure under acute and chronic oral levodopa therapy.
Catecholamine metabolism was assessed in 14 patients with chronic congestive heart failure (NYHA class IV; cardiac index 2.4 +/- 0.2 l min-1, ejection fraction 20 +/- 11%) on levodopa (L-Dopa-ratiopharm) treatment: 1. prior to the start of levodopa treatment; 2. following acute administration of levodopa in the 14 patients and in 4 healthy control subjects; 3. after 30 days +/- 1 day with 2-4 g levodopa p.o. daily in the group of patients. Only a minority of the patients showed sustained clinical and/or hemodynamic improvement. Free and conjugated plasma dopamine and urinary/excretion of dopamine increased 20- to 40-fold in the group of patients and in the healthy control subjects subsequent to levodopa administration. An increase in noradrenaline and adrenaline levels (conjugated plasma fractions and urinary excretion of free noradrenaline and adrenaline) was only observed in the healthy control subjects, but not in the group of patients. Free noradrenaline and adrenaline plasma fractions did not show any significant change on levodopa treatment, either in the group of patients or in healthy control subjects. Clinical and hemodynamic changes seen on levodopa treatment are related to elevated dopamine concentrations. The lack of increase in noradrenaline and adrenaline in the group of patients may be related to reduced activity of dopamine-beta-hydroxylase in patients with congestive heart failure NYHA class IV.
Administration, Oral↗
[Transesophageal and Doppler ultrasound studies before and following percutaneous balloon valvuloplasty of the aortic valve].
Transesophageal and Doppler-echocardiography were performed in 25 patients with severe valvular aortic stenosis before and after percutaneous balloon valvuloplasty. The maximal systolic gradient over the aortic valve determined during invasive measurements before and after valvuloplasty decreased from 71 +/- 24 mm Hg to 36 +/- 14 mm Hg; the mean systolic gradient decreased from 53 +/- 18 mm Hg to 28 +/- 10 mm Hg. The aortic orifice area increased from 0.67 +/- 0.2 to 0.94 +/- 0.2 cm2. During transesophageal echocardiography the aortic orifice area was calculated by direct planimetry. The aortic valve area increased from 0.52 +/- 0.21 cm2 before the valvuloplasty to 0.72 +/- 0.17 cm2 after intervention. After valvuloplasty small thrombotic vegetations were observed in four patients and valvular lesions in two patients. Using Doppler-echocardiographic measurements to quantify the aortic valve stenosis the maximal instantaneous gradient decreased from 94 +/- 30 before valvuloplasty to 66 +/- 25 mm Hg after valvuloplasty; the mean instantaneous gradient changed from 52 +/- 17 to 37 +/- 14 mm Hg. The aortic orifice area increased from 0.5 +/- 016 to 0.76 +/- 0.21 cm2. These results confirm that transesophageal and Doppler-echocardiography are appropriate to control the success of percutaneous balloon valvuloplasty.
Aged↗
[Predictive value of programmed electrostimulation in patients with spontaneous idiopathic ventricular tachycardia].
In contrast to patients with organic heart disease, there are only few data available on the incidence and type of inducible arrhythmias during programmed electrical stimulation (PES) in patients with spontaneous ventricular tachycardia (VT) but without evidence of underlying heart disease. Additionally, no consensus has been achieved in these patients on the most appropriate stimulation protocol required to reproduce the clinical arrhythmia. In a prospective study we analyzed in 40 patients without idiopathic VT, incidence and type of inducible VT, as well as the mode of initiation during a right ventricular PES protocol with 1-2 (part I) and three extrastimuli (part II). Twelve patients had spontaneous sustained monomorphic VT (group A), 28 patients were studied with spontaneous non-sustained VT (group B). During PES, a non-sustained polymorphic VT was induced in 3/12 patients (group A, 25%) and in 10/28 patients (group B, 36%); a non-sustained monomorphic VT was induced in 5/12 patients (group A, 41%) and in 4/28 patients (group B, 14%). In all 7/12 patients (59%) of group A with inducible sustained monomorphic VT, the arrhythmia was initiated with 1-2 extrastimuli. In group B, only 2/28 patients (7%) were induced to a sustained monomorphic VT. When the clinical arrhythmia was exercise-related, 5/6 patients (83%) in group A and 7/13 patients (54%) in group B were induced to a VT, while 2/6 patients (33%) in group A and 1/13 (8%) patients in group B were induced to a sustained monomorphic VT. Isoprenaline was not effective to increase the incidence of sustained monomorphic VT.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
[Transfemoral, transatrial double-balloon valvuloplasty of rheumatic mitral stenosis].
A percutaneous transfemoral, transatrial double-balloon valvuloplasty was performed on 21 patients (53 +/- 14 years) with rheumatic mitral stenosis. An open commissurotomy was performed in six patients, 20 +/- 9 years previously; in three patients an arterial embolism had occurred previously. Balloon valvuloplasty resulted in a reduction of the mean diastolic gradient from 16 +/- 7 to 8 +/- 3 mm Hg (p less than 0.001), and the mitral valve orifice area increased from 1.1 +/- 0.3 to 2.2 +/- 0.8 cm2 (p less than 0.001). Mitral insufficiency increased in three patients and was first observed after valvuloplasty in four patients. Complications were seen in three patients: a left ventricular perforation resulting in pericardial tamponade occurred in two patients, which required cardiothoracic intervention. In one patient a pulmonary embolism occurred five days after the invasive procedure. The study shows that percutaneous transfemoral balloon valvuloplasty can successfully be performed in patients with severe or even calcified mitral valve stenosis. The risk of severe complications is, however, not negligible.
Adult↗
Incidence and clinical relevance of QT prolongation caused by the new selective serotonin antagonist ketanserin.
Efficacy and safety of ketanserin were studied prospectively in a randomized, double-blind trial involving 221 patients treated for hypertension or coronary artery disease, or both. Since ketanserin has been suggested to cause QTc prolongation, the incidence and severity of this effect were investigated, as was the incidence of malignant ventricular arrhythmias during Holter monitoring. After a 1-week run-in period, all patients were examined: blood pressure was measured and electrocardiograms and 24-hour Holter electrocardiograms were obtained. Two thirds of the patients (n = 147) were then randomized to receive ketanserin for 1 week (20 mg twice daily) followed by 3 weeks of 40 mg twice daily; one third of the patients (n = 74) received placebo (twice daily) for 4 weeks. After 4 weeks of treatment, blood pressure, electrocardiograms and 24-hour Holter electrocardiograms were repeated. In hypertensive patients, ketanserin significantly reduced systolic (mean reduction 17 +/- 2 mm Hg, p less than 0.0001) and diastolic blood pressure (12 +/- 1 mm Hg, p less than 0.0001) compared to baseline, and to the placebo group (p less than 0.005 for systolic and diastolic blood pressure). The QTc interval was prolonged with ketanserin (mean 400 to 418 ms, p less than 0.01) but not with placebo (399 vs 402 ms). In the ketanserin group 30% of patients and in the placebo group 8% of patients had QTc prolongation greater than 30 ms (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Comparison of twice daily with thrice daily administered encainide for benign or potentially lethal ventricular arrhythmias.
The antiarrhythmic efficacy of encainide administered 2 (group A) or 3 times daily (group B) was evaluated in a randomized, placebo-controlled trial involving 101 patients with benign or potentially malignant ventricular arrhythmias. In group A, encainide was titrated at dosages of 35, 50 and 75 mg twice daily and in group B at dosages of 25, 35 and 50 mg 3 times daily. Drug efficacy, as judged by repeated ambulatory monitoring, was defined as greater than 75% reduction in ventricular premature complexes combined with a greater than 90% abolition of pairs and runs of nonsustained ventricular tachycardia. In group A, 27 of 52 patients (52%) had their arrhythmia suppressed by the drug compared with 34 of 49 (69%) in group B (difference not significant). There was a trend toward better arrhythmia control in group B if a total daily dose of greater than 100 mg was necessary for arrhythmia suppression. Side effects were frequent in both groups (24 vs 28%, difference not significant). Thus, encainide administered twice daily effectively suppresses ventricular arrhythmias in this patient population.
Adult↗
Dopexamine in congestive heart failure: how do the pharmacological activities translate into the clinical situation?
Dopexamine is a newly developed sympathetic catecholamine which combines dopaminergic (DA-1) and beta 2-adrenergic agonist activity with only minor beta 1-adrenergic action. Thereby, this compound exerts systemic and preferential renal vasodilation, causing afterload reduction, increases in cardiac output, and improved renal perfusion in animals and normal volunteers. Short-term administration of dopexamine in congestive heart failure established beneficial effects in central hemodynamics, that is, reduction of systemic and pulmonary vascular resistance, combined with a decrease in LV-filling pressures and increased renal blood flow. The effect on central hemodynamics are comparable to sodium nitroprusside. With higher doses, however, heart rate may increase substantially with dopexamine along with increased myocardial oxygen consumption. Experiences with prolonged administration of this drug are scarce and have, so far, yielded conflicting results. Thus, dopexamine appears to be a promising agent in the short-term management of congestive heart failure. However, its ultimate value for prolonged administration remains to be established.
Adrenergic Agonists↗
Diagnosis of hidden pacemaker lead sepsis by transesophageal echocardiography and a new technique for lead extraction.
Explore the source record for details and available documents.
Aged↗
Percutaneous recanalization and dilatation of a thrombotically occluded superior vena cava in a patient with a peritoneovenous shunt.
A superior vena cava syndrome developed in a patient with liver cirrhosis 6 months after implantation of a peritoneovenous shunt. Local fibrinolytic therapy resulted only in a transient improvement of clinical symptoms. Persistent patency of the superior vena cava and shunt function was regained only after percutaneous recanalization and balloon dilatation of the thrombotically occluded caval vein.
Angiography↗
Antiarrhythmic efficacy and tolerance of oral propafenone in patients with frequent ventricular arrhythmias: experience of a multicentre study.
In a multicentre study efficacy and safety of propafenone 450 mg day-1 and 750 mg day-1 was studied in 97 patients with frequent ventricular premature beats (VPB greater than 30 h-1). 70 patients suffered from organic heart disease, in 27 patients no organic heart disease was present during an initial work-up. After a 1-week washout period, all patients underwent 24 h Holter monitoring. Patients were then treated by propafenone 450 mg day-1 and controlled for 24 h Holter, ECG, blood pressure, blood chemistry and side-effects after 1 week of treatment. At this time, 35 patients were responders (reduction of VPB greater than 84%, of ventricular pairs greater than 90% and of ventricular tachycardia 100%). The mean reduction of VPB in all patients was 60%, of ventricular pairs 88% and of ventricular tachycardia 100%. When treatment was continued for 3 weeks 20/35 patients (56%) were still responders. The mean reduction of VPB was 83%. In 42 non-responders to 450 mg day-1 the dose was increased to 750 mg day-1. Of these patients, 17 (41%) became responders after 3 weeks of treatment; the mean reduction of VPB increased from 17% (first week, 450 mg day-1) to 63% (750 mg day-1). Ventricular pairs were reduced by 80%, ventricular tachycardia by 100%. Side-effects occurred in 11/97 patients and limited therapy in six patients. The most frequent complaints were dryness of the mouth, nausea, tiredness, headache and gastrointestinal upset. In conclusion, propafenone in a dose of 450-750 mg day-1 seems to be an effective and safe antiarrhythmic agent in the majority of patients.
Administration, Oral↗
Contrasting peripheral short-term and long-term effects of converting enzyme inhibition in patients with congestive heart failure. A double-blind, placebo-controlled trial.
To discover the underlying mechanisms involved in the beneficial long-term effects of angiotensin converting enzyme (ACE) inhibitors, we investigated the systemic and peripheral effects of short- and long-term ACE inhibition in patients with chronic heart failure. After assessing the short-term effects and dose titration with cilazapril, a new long-acting ACE inhibitor, 21 patients were randomized to receive either placebo or the ACE inhibitor. Seventeen patients completed the 3-month treatment. Central hemodynamic output, femoral blood flow (measured by thermodilution), oxygen saturation, and lactate and norepinephrine levels were determined simultaneously in the femoral vein and radial artery during treatment and after a 3-month rest and during symptom-limited bicycle exercise. Short-term ACE inhibition improved rest and exercise hemodynamic output, but it did not alter peak femoral blood flow, calculated leg oxygen consumption, or systemic oxygen uptake during exercise, despite significant reduction in femoral norepinephrine extraction and arterial angiotensin levels during exercise. In contrast, long-term ACE inhibition further improved exercise cardiac output and increased leg blood flow (from 2.3 to 2.9 l/min, p less than 0.05), leg oxygen consumption (from 277 to 403 ml/min, p less than 0.05), and systemic oxygen uptake (from 1,133 to 1,453 ml/min, p less than 0.05), whereas these variables remained unchanged with placebo treatment (p less than 0.02 between groups). Moreover, a moderate but significant increase in femoral oxygen extraction occurred after long-term therapy (ACE inhibitor: from 76% to 83%, p less than 0.05; placebo: from 75% to 74%, NS; p less than 0.01 between groups). We conclude that long-term ACE inhibition is clinically beneficial in that it improves blood flow to skeletal muscle during exercise over time. The long-term effects of ACE inhibition are, in part, probably related to peripheral (vascular) mechanisms, for example, by reversing the inability of peripheral vessels to dilate and by improving oxygen utilization.
Angiotensin-Converting Enzyme Inhibitors↗
Myocardial energetics in patients with dilated cardiomyopathy. Influence of nitroprusside and enoximone.
Cardiotonic agents influence myocardial energy consumption by vasodilation, which may reduce energy demand, and by inotropism, which may increase it. To distinguish between the two effects, myocardial oxygen consumption must be analyzed in relation to its hemodynamic determinants. The coupling of myocardial oxygen consumption with its determinants was investigated in 22 patients with idiopathic dilated cardiomyopathy (NYHA Class II and III). Predicted myocardial oxygen consumption by the pressure-work index, the Bretschneider index, and the pressure-volume area correlated moderately with measured myocardial oxygen consumption (r = 0.57, p less than 0.001; r = 0.52, p less than 0.005; and r = 0.63, p less than 0.001). Multiple regression analysis, including left ventricular peak systolic wall stress, systolic stress-time integral, pressure-volume work, maximum rate of left ventricular pressure rise, and mean velocity of circumferential fiber shortening indicated that systolic stress-time integral is the major determinant of myocardial oxygen consumption (r = 0.75, p less than 0.001) in these patients. Enoximone, a phosphodiesterase inhibitor, has an inotropic and a vasodilating effect. To investigate the inotropic portion of the energy cost of this phosphodiesterase inhibitor, the influence of enoximone on myocardial oxygen consumption and systolic stress-time integral was compared with the effects of nitroprusside, which is a vasodilator only. Nitroprusside (10 patients) and enoximone (12 patients) reduced left ventricular systolic stress-time integral from 109 +/- 22 to 71 +/- 21 (p less than 0.005) and from 104 +/- 23 to 42 +/- 10 (p less than 0.001) 10(3) dynes.sec/cm2, respectively. Myocardial oxygen consumption decreased from 159 +/- 44 to 112 +/- 23 (p less than 0.005) and from 134 +/- 28 to 109 +/- 21 (p less than 0.001) microliters/beat/100 g, respectively. In both groups, there was a significant correlation between the decrease in myocardial oxygen consumption and the decrease in systolic stress-time integral. The slopes of the respective linear regression lines were significantly different (1.27 for nitroprusside and 0.51 nl.cm2/100 g.dynes.sec for enoximone, p less than 0.05), indicating a smaller decrease of myocardial oxygen consumption for a given decrease of stress-time integral with enoximone. Applying the pressure-work index or the pressure-volume area instead of systolic stress-time integral yielded comparable results. Thus, vasodilation reduces myocardial oxygen consumption in proportion to the reduction of stress-time integral. With enoximone, the energy-saving effect of vasodilation is counteracted in part by the increased energy d
Adult↗
Flow-dependent coronary artery dilatation in humans.
To determine the role of endothelium-mediated flow-dependent coronary dilatation in humans, we studied the coronary dilatation exerted by maximal pharmacologic increase of coronary flow in 14 patients with normal coronary arteries. Biplane views of the circumflex (Cx) and left anterior descending (LAD) coronary arteries were obtained before and 80 seconds after inducing a maximal increase in flow selectively in the Cx by injecting 7 mg papaverine through a 2F infusion catheter in the midportion of the Cx (n = 10). The diameter of the proximal Cx segment (exposed to increased flow but not to papaverine directly) increased with papaverine by 11.1 +/- 4% (range, 5.2-16.4%, p less than 0.001 vs. control), whereas the LAD diameter did not change. LAD and Cx diameters increased by 18.3% and 21.2% after nitroglycerin given into the left main artery, which showed the preserved capability of the LAD to dilate. In four patients with normal coronary arteries and six patients with coronary artery disease (CAD, non-flow-limiting stenosis), a similar protocol was applied with the LAD for the assessment of flow-dependent dilatation. Simultaneously, intracoronary blood flow velocity was measured by an intracoronary Doppler catheter. Papaverine-induced coronary flow reserve (peak/resting velocity ratio) in the LAD was 4 +/- 0.7 (range, 3.5-5) in normal arteries and was 3.5 +/- 0.6 (range, 2.7-4.4) in CAD.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗