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B Lamp

Publications and source records attributed to B Lamp.

13 recordsLinked to original sources

[Left ventricular pacing and CRT. What CV lead fits into which vein?].

The experience of 579 patients with left ventricular pacing specific characteristics of various leads and lead types for left ventricular stimulation are reported. After describing the advantages of coronary vein (CV) leads versus epicardial lead usage for left ventricular stimulation, commercially available CV leads are introduced and discussed. Since there is no universally applicable CV lead, the individual optimal lead choice and the sequelae of erroneous lead choice are described in typical clinical examples.

Cardiac Catheterization↗

Cardiac re-synchronization therapy: effects on myocardial perfusion at rest, after vasodilation and oxygen consumption.

AIM: Cardiac resynchronization therapy (CRT) has been shown to improve haemodynamics and clinical symptoms in heart failure patients. The present study evaluated the effects of a 4-month CRT on myocardial blood flow (MBF) at rest, after vasodilation and on myocardial oxygen consumption (MVO(2)). PATIENTS, METHODS: We studied 16 patients with idiopathic dilated cardiomyopathy prior to and during CRT performed as biventricular pacing. Resting MBF and MVO(2) were determined from an (11)C-acetate PET study and vasodilator MBF from a (13)N-ammonia study. RESULTS: MBF at rest (0.55 +/- 0.10 ml/min/g), after vasodilation (1.20 +/- 0.45 ml/min/g), and MVO2 (0.082 +/- 0.014/min) did not change by mid-term CRT at a global level (0.57 +/- 0.11 ml/min/g; 1.32 +/- 0.49 ml/min/g; 0.085 +/- 0.018/min), whereas the rate pressure product (RPP) normalised MVO(2) decreased from 0.104 +/- 0.024 to 0.086 +/- 0.018/min (p = 0.02). At baseline, the regional analysis revealed significantly higher values for all parameters in the lateral wall than for those in the other walls. Under CRT the regional differences between the resting parameters equalized and all parameters showed significant lower coefficients of variation. CONCLUSION: Effects of mid-term CRT on resting MBF, vasodilator MBF and MVO(2) occur at a regional level. The resynchronization is associated with a more homogenous distribution pattern of these parameters among the myocardial walls. Substantial alterations to global MBF at rest, after vasodilation or to MVO(2) are not detectable. Regarding the RPP normalised MVO(2), there is evidence of improved ventricular efficiency through CRT.

Aged↗

[Acute hemodynamic effects].

Several studies on the acute effect of cardiac resynchronization in patients with advanced heart failure (HF) and left bundle branch block (LBBB) have shown that left and biventricular stimulation increase pulse pressure and contractility, while patients with a QRS complex <150 ms may deteriorate during stimulation. Patients with LBBB, severe HF and a QRS width >150 ms underwent right, left and biventricular stimulation at different AV delays. Acute response was defined as > or =10% pulse pressure increase. 165 of 188 patients (88%) in sinus rhythm (47 women, mean age 62.5+/-10 years, ejection fraction 23+/-8%, NYHA class 3.1+/-0.3) were regarded acute responders. 10% of 103 patients with dilated cardiomyopathy and 16.5% of 79 patients with coronary artery disease were considered non-responders. 29 patients (81%) with 2 posterolateral veins were acute responders with 10 of them (33%) being responders in only one vein. 54 patients had a higher pulse pressure increase (10.7+/-10.6%) with atrio-left ventricular stimulation, 48 patients with atrio-biventricular stimulation (9.8+/-6.4%). At one-year follow-up, heart failure had significantly (p<0.0001) improved from NYHA class 3.1+/-0.4 to 2.1+/-0.7, VO(2)peak from 12.7+/-2.8 to 15.9+/-3.6 ml/min/kg. Left ventricular enddiastolic diameter being an indicator of reverse remodeling decreased from 80.5+/-10.5 to 73.3+/-13 (p<0.0001). Hemodynamic testing before CRT allows for the identification of acute non-responders as well as the best mode and site of stimulation and the optimal atrioventricular delay in responders.

Arrhythmia, Sinus↗

[Analysis of inter- and intraventricular asynchrony by tissue Doppler echocardiography].

BACKGROUND AND INTRODUCTION: Cardiac resynchronization therapy (CRT) is a promising non-pharmacological treatment option for patients (pts) with severe severe heart failure (CHF), systolic left ventricular (LV) dysfunction, and ventricular conduction abnormalities (VCA). Pt selection for CRT, however, is still controversial. Tissue Doppler echocardiography (TDE) can be used to analyze regional wall motion with high temporal resolution. PATIENTS AND METHODS: In 33 CHF pts with VCA (QRS width > or =140 ms) and 20 normal probands, left and right ventricular (RV) filling and emptying were analyzed by flow and tissue Doppler to assess regional (anterior, lateral, inferior, and septal) asynchrony within the LV as well as asynchrony between the RVand LV. All time measurements were corrected for a heart rate of 60 bpm. Results Maximum interventricular and segmental intraventricular delay was 30 ms in the normals. LV asynchrony, defined as a regional delay of > or =40 ms, was found in 29/33 (88%) of the CHF pts, in 4 cases there was synchronous LV contraction despite VCA. In the pts with LV asynchrony, 22 (67%) showed the maximum delay in the lateral wall, 7 (21%) in the septum. Inter- and intra-ventricular asynchrony correlated weakly. CONCLUSIONS: In many CHF pts with VCA, there is a delay both between the two ventricles, and among different LV regions. Predominantly but not exclusively, the LV lateral wall shows the maximum intra-LV delay. Some CHF pts, however, seem to have a synchronous LV contraction despite VCA. TDE thus adds important information for pt selection with respect to CRT.

Adult↗

Electrocardiographic remodeling in patients paced for heart failure.

Congestive heart failure due to advanced coronary artery disease or dilated cardiomyopathy is often associated with intraventricular conduction delays. Electrical resynchronization is an evolving method to improve clinical and functional status. To evaluate whether pacing-induced changes in the electrocardiogram are related to hemodynamic changes, we analyzed electrocardiograms of patients enrolled in the Pacing Therapies in Congestive Heart Failure trial. The study population consisted of 42 patients, New York Heart Association functional class III-IV with a baseline QRS complex of 175 +/- 32 msec and a PR interval of 196 +/- 33 msec. The mean left ventricular ejection fraction was 0.23. Using high-resolution computer scans, we measured QRS duration of intrinsic and paced electrocardiographs at different times during the study. Results of the electrocardiographic measurements were correlated with functional results. During the crossover period, 34 episodes of biventricular pacing, 27 episodes of left ventricular pacing, and 5 episodes of right ventricular pacing occurred, each at an individual optimized atrioventricular (AV) delay. The only significant difference was that right ventricular pacing increased the QRS width by 40 msec as compared with baseline or biventricular pacing. Functional benefit, as indicated by relative increase of peak oxygen uptake (VO2) compared with baseline, was significantly correlated with shortening of paced QRS width (correlation coefficient, r = 0.55; p <0.05). After 12-month follow-up of 28 patients, we saw a slight, nonsignificant decrease of intrinsic QRS width. With regard to the underlying disease, intrinsic QRS width at baseline and at 12 months was also not significantly different between patients with coronary artery disease and dilated cardiomyopathy. This study found that right ventricular pacing causes an increase in QRS duration in patients with left bundle-branch block, whereas in left ventricular and biventricular pacing, QRS width remains unchanged. Shortening of QRS width is correlated with a pronounced relative increase of peak VO2, and thus may become a noninvasive marker of clinical efficacy. There is no evidence of remodeling of the intrinsic electrocardiogram after 12 months of pacing.

Arrhythmias, Cardiac↗

Fractally coated defibrillation electrodes: is an improvement in defibrillation threshold possible?

AIMS: In patients with implantable cardioverter-defibrillators (ICD), the goals of lowering the defibrillation threshold (DFT) can be achieved by means of higher defibrillation safety margins, more rapid charging of capacitors, improved battery longevity, implying smaller devices. Whether an increase in the electrically active surface of ICD leads by fractal coating results in decreased DFTs is unknown. METHODS AND RESULTS: In this prospective randomized cross-over study the defibrillation efficacy of a novel right ventricular endocardial defibrillation electrode fractally coated with iridium was compared with an uncoated but otherwise identical electrode in 30 patients undergoing ICD implantation. In each patient, DFT testing was performed twice according to a binary search protocol introducing the two different electrodes in a random order. The mean DFT was 8.4 +/- 4.1 J with the fractally coated lead and 9.6 +/- 3.6 J using the uncoated lead. The improvement of 1.2 J was statistically not significant (P = 0.11). No differences were observed between the patients with an improved DFT (n =12) and those with an unchanged or worsened DFT (n = 18) concerning age, underlying cardiac disease, NYHA class, or left ventricular ejection fraction, respectively. CONCLUSION: Increasing the electrical surface of defibrillation leads by fractal coating does not lead to a substantial clinically relevant reduction in defibrillation thresholds. Defibrillation impedance is not influenced by the increased electrical surface of the defibrillation lead.

Adult↗

Multiple hardware complications in a patient with an ICD.

Hardware-related complications in implantable cardioverter/defibrillators (ICD) are still a common problem. Identifying underlying reasons becomes more and more difficult as the complexity of ICD systems increases. We report a patient with a dual chamber ICD (DDD-ICD) who suffered multiple complications. These included: ventricular oversensing causing inappropriate shocks and episodes of asystole; an insulation defect resulting in ineffective shocks as a consequence of a short circuit between the active can device and a defective high voltage cable; and device dysfunction requiring several hospitalizations and operative system revisions.

Aged↗

[Initial experiences with dobutamine stress echocardiography in heart transplant patients].

UNLABELLED: Cardiac allograft vasculopathy (CAV) has become one of the primary obstacles to long-term survival of patients after heart transplantation. The low sensitivity of currently available noninvasive tests still remains a problem in the early diagnosis of the disease. To assess the feasibility, safety, and usefulness of dobutamine stress echocardiography as a noninvasive predictor of cardiac allograft vasculopathy, we examined 20 patients (3 female) 3-35 months after orthotopic heart transplantation. All patients underwent coronary angiography within 2 weeks of dobutamine stress echocardiography. RESULTS: 89% of the segments examined could be evaluated for wall motion abnormalities. Under increasing doses of dobutamine (5 to max. 30 micrograms/kg/min), heart rate increased from 88 +/- 13 bpm to 141 +/- 16 bpm. and systolic blood pressure from 139 +2- 14 mm Hg to 154 +/- 28 mm Hg. Two of 4 patients with angiographically detected CAV developed new wall motion abnormalities under dobutamine; their wall motion score increased from 1.23 +/- 0.22 to 1.31 +/- 0.24. In the other patients without CAV, the wall motion score remained almost unchanged (1.01 +/- 0.3 to 1.02 +/- 0.4). Dobutamine was well tolerated, and there were no serious complications. Thus, dobutamine stress echocardiography seems to be feasible and safe in patients after heart transplantation. Our results suggest that it might be useful for the detection of cardiac allograft vasculopathy. The final determination of its clinical usefulness in the diagnosis of cardiac allograft vasculopathy needs further extensive investigations.

Adult↗

Clinical significance and management of ventricular arrhythmias in heart failure.

Ventricular arrhythmias are a frequent finding in patients with heart failure, and heart failure is a major underlying condition which is correlated to sudden death. Therefore, both sudden death and death from progression of heart failure strongly overlap. Besides long-term ECG recording, newer diagnostic techniques have been developed. The prognostic significance of the signal-averaged ECG in patients with advanced left ventricular dysfunction in the presence of coronary artery disease has been demonstrated; however, in patients with dilated cardiomyopathy, signal-averaging for detection of late potentials has not yet been clearly established as a useful diagnostic tool. Furthermore, heart period variability has been shown to correlate to overall mortality but not to a specific mechanism. Finally, programmed ventricular stimulation, though useful in patients with left ventricular dysfunction and/or heart failure in the setting of coronary artery disease, is of questionable significance in patients with dilated cardiomyopathy. With increasing degrees of left ventricular dysfunction, the efficacy of antiarrhythmic drugs decreases. On the other hand, with increasing degrees of heart failure, antiarrhythmic drugs demonstrate a greater negative inotropic effect, more frequent proarrhythmic effects, and more frequent bradyarrhythmias. Currently, several ongoing amiodarone trials are assessing different approaches of antiarrhythmic treatment in patients with heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Allograft vasculopathy in the early phase of orthotopic heart transplantation: angiography, intravascular ultrasound and functional in vivo findings].

Accelerated graft coronary atherosclerosis disease is the main reason for long-term mortality and morbidity of heart transplant recipients. The aim of this in vivo study was to evaluate coronary atherosclerotic vessel abnormalities and endothelial function using angiography, intravascular ultrasound, and intracoronary acetylcholine infusion. Fourteen patients (11 male, 3 female; mean age 49.3 years) were examined early after heart transplantation (mean interval after transplantation: 11 weeks) because of coronary artery disease (n = 8), idiopathic dilatative cardiomyopathy (n = 7), mitral valve replacement (n: 1) or left atrial filiae of a leiomyosarcoma (n = 1). Mean age of the donor hearts (female n = 8) was 29 years; 3 patients received double- and 14 patients triple-immunosuppression. All patients underwent biplane ventriculography and coronary angiography; a total of 120 coronary segments (main stem 21, left anterior descending artery 85, circumflex artery 14) was examined by intravascular ultrasound (20 MHz, 3.5 F catheters). In 13 patients, acetylcholine was infused into the proximal left anterior descending artery (0.15 microgram/min to 150.0 micrograms/min) to evaluate vasomotion within this segment. Ventriculography demonstrated regional wall abnormalities in 2 patients, angiography revealed 9 noncritical stenotic segments in 5 patients. Intravascular ultrasound detected 52 cross-sectional areas with a three-layer appearance indicating intimal thickening. Mean circumferential expansion of intimal proliferation was 192 degrees and mean intimal thickness was 0.35 mm. Only 5 segments of the sonographically pathological cross-sectional areas showed angiographic evidence of atherosclerotic lesions. After intracoronary infusion at a lower dose (0.15 and 1.5 micrograms/min) of acetylcholine, vasoconstriction was observed in 2 patients, at a dose of 15.0 and 150.0 micrograms/min in 10 patients. This response to acetylcholine did not depend on the intravascular or angiographical extent of atherosclerotic vessel abnormalities. In heart transplant recipients, coronary artery abnormalities can already be depicted at an early stage using intravascular ultrasound. The majority of patients show coronary vasoconstriction following infusion of acetylcholine at a higher dose. Further investigation is necessary to clarify whether the depicted vessel wall abnormalities can already be interpreted as newly developed graft atherosclerosis and whether abnormal vasomotion after acetylcholine is indicative of endothelial dysfunction.

Acetylcholine↗

Modulation of calcium ion influx by the 1,4-dihydropyridines nifedipine and BAY K 8644.

We examined the effects of the new dihydropyridine calcium agonist BAY K 8644 on calcium influx and mechanical activity in rabbit aortic rings and compared them with those of the classical calcium antagonist nifedipine. The vasodilating effects of nifedipine and the vasoconstricting effects of BAY K 8644 can be explained by the calcium influx modulating activity of these two dihydropyridines. Only at the high concentration of 3 X 10(-6) mol/L BAY K 8644 is there a marked difference between increased calcium influx and reduced contraction.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗