About: Artificial cardiac pacemaker is a research topic. Over the lifetime, 356 publications have been published within this topic receiving 8398 citations. The topic is also known as: artificial cardiac pacemaker & pacemaker.
TL;DR: In this paper, the authors conducted a meta-analysis of randomized controlled trials to determine whether cardiac resynchronization reduces mortality from progressive heart failure in patients with symptomatic left ventricular dysfunction.
Abstract: ContextProgressive heart failure is the most common mechanism of death among
patients with advanced heart failure. Cardiac resynchronization, a pacemaker-based
therapy for heart failure, enhances cardiac performance and quality of life,
but its effect on mortality is uncertain.ObjectiveTo determine whether cardiac resynchronization reduces mortality from
progressive heart failure.Data SourcesMEDLINE (1966-2002), EMBASE (1980-2002), the Cochrane Controlled Trials
Register (Second Quarter, 2002), The National Institutes of Health ClinicalTrials.gov
database, the US Food and Drug Administration Web site, and reports presented
at scientific meetings (1994-2002). Search terms included pacemaker, pacing, heart
failure, dual-site, multisite, biventricular, resynchronization, and left ventricular preexcitation.Study SelectionEligible studies were randomized controlled trials of cardiac resynchronization
for the treatment of chronic symptomatic left ventricular dysfunction. Eligible
studies reported death, hospitalization for heart failure, or ventricular
arrhythmia as outcomes. Of the 6883 potentially relevant reports initially
identified, 11 reports of 4 randomized trials with 1634 total patients were
included in the meta-analysis.Data ExtractionTrial reports were reviewed independently by 2 investigators in an unblinded
standardized manner.Data SynthesisFollow-up in the included trials ranged from 3 to 6 months. Pooled data
from the 4 selected studies showed that cardiac resynchronization reduced
death from progressive heart failure by 51% relative to controls (odds ratio
[OR], 0.49; 95% confidence interval [CI], 0.25-0.93). Progressive heart failure
mortality was 1.7% for cardiac resynchronization patients and 3.5% for controls.
Cardiac resynchronization also reduced heart failure hospitalization by 29%
(OR, 0.71; 95% CI, 0.53-0.96) and showed a trend toward reducing all-cause
mortality (OR, 0.77; 95% CI, 0.51-1.18). Cardiac resynchronization was not
associated with a statistically significant effect on non–heart failure
mortality (OR, 1.15; 95% CI, 0.65-2.02). Among patients with implantable cardioverter
defibrillators, cardiac resynchronization had no clear impact on ventricular
tachycardia or ventricular fibrillation (OR, 0.92; 95% CI, 0.67-1.27).ConclusionsCardiac resynchronization reduces mortality from progressive heart failure
in patients with symptomatic left ventricular dysfunction. This finding suggests
that cardiac resynchronization may have a substantial impact on the most common
mechanism of death among patients with advanced heart failure. Cardiac resynchronization
also reduces heart failure hospitalization and shows a trend toward reducing
all-cause mortality.
TL;DR: Pacemaker therapy is of clinical and haemodynamic benefit for patients with hypertrophic obstructive cardiomyopathy, left ventricular outflow gradient at rest over 30 mmHg who are symptomatic despite drug treatment.
Abstract: Background Uncontrolled studies have shown that short atrioventricular delay dual chamber pacing reduces outflow tract obstruction in hypertrophic obstructive cardiomyopathy. Although the exact mechanism of this beneficial effect is unclear, this seems a promising potential new treatment for hypertrophic obstructive cardiomyopathy.
Method In order to evaluate the impact of pacing therapy, we performed a randomized multicentre double-blind crossover (pacemaker activated vs non activated) study to investigate modification of echocardiography, exercise tolerance, angina, dyspnoea and quality of life in 83 patients with a mean age of 53 (range 22–87) years with symptoms refractory or intolerant to classical drug treatment.
Results After 12 weeks of activated or inactivated pacing, independent of which phase was first, the pressure gradient fell from 59±36 mmHg to 30±25 mmHg ( P <0·001) with active pacing.
Exercise tolerance improved by 21% in those patients who at baseline tolerated less than 10 min of Bruce protocol; symptoms of dyspnoea and angina also improved significantly from NYHA class 2·4 to 1·4 and 1·0 to 0·4, respectively ( P <0·007). Quality of life assessment with a validated questionnaire objectivated the subjective improvement.
Conclusion Pacemaker therapy is of clinical and haemodynamic benefit for patients with hypertrophic obstructive cardiomyopathy, left ventricular outflow gradient at rest over 30 mmHg who are symptomatic despite drug treatment.
TL;DR: Left bundle branch pacing that has a low pacing threshold and produces narrow ECG QRS duration may be a new pacing strategy for patients in need of ventricular pacing.
Abstract: AIMS This study explores the feasibility of left bundle branch pacing (LBBP) and characterizes electrocardiogram (ECG) patterns during the pacing in comparison with conventional right ventricular pacing (RVP). METHODS AND RESULTS Forty pacing-indicated patients were prospectively enrolled. Twenty patients underwent LBBP (the LBBP group), and 20 patients underwent RVP (the RVP group). Left bundle branch pacing was achieved by transseptal method in the basal ventricular septum. Electrocardiogram characteristics, pacing parameters, pacing sites, and safety events were assessed at implantation and 3-month follow-up. In the LBBP group, the pacing lead was successfully placed near the endocardium of the left side of the septum. Electrocardiogram pattern during LBBP showed right bundle branch conduction delay. Left bundle branch block (LBBB) in two patients was corrected by LBBP. Post-implantation 3D echocardiography confirmed the pacing location. In the RVP group, ECG showed LBBB pattern. The paced QRS duration was 111.85 ± 10.77 ms in LBBP group and 160.15 ± 15.04 ms in the RVP group (P < 0.001). Pacing thresholds (at implantation: 0.73 ± 0.20 V in the LBBP group and 0.61 ± 0.23 V in the RVP group) remained low and stable at 3-month follow-up. No adverse event was observed during 3-month follow-up. CONCLUSION This study demonstrates the clinical feasibility of LBBP. Left bundle branch pacing that has a low pacing threshold and produces narrow ECG QRS duration may be a new pacing strategy for patients in need of ventricular pacing.
TL;DR: Evidence is accumulating that microvolt T wave alternans is a marker of increased risk for ventricular tachyarrhythmias, and a noninvasive approach has been developed that elevates heart rate using exercise.
Abstract: INTRODUCTION: Evidence is accumulating that microvolt T wave alternans (TWA) is a marker of increased risk for ventricular tachyarrhythmias. Initially, atrial pacing was used to elevate heart rate and elicit TWA. More recently, a noninvasive approach has been developed that elevates heart rate using exercise. METHODS AND RESULTS: In 30 consecutive patients with a history of ventricular tachyarrhythmias, the spectral method was used to detect TWA during both atrial pacing and submaximal exercise testing. The concordance rate for the presence or absence of TWA using the two measurement methods was 84%. There was a patient-specific heart rate threshold for the detection of TWA that averaged 100 +/- 14 beats/min during exercise compared with 97 +/- 9 beats/min during right atrial pacing (P = NS). Beyond this threshold, there was a significant and comparable increase in level of TWA with decreasing pacing cycle length and increasing exercise heart rates. CONCLUSIONS: The present study is the first to demonstrate that microvolt TWA can be assessed reliably and noninvasively during exercise stress. There is a patient-specific heart rate threshold beyond which TWA continues to increase with increasing heart rates. Heart rate thresholds for the onset of TWA measured during atrial pacing and exercise stress were comparable, indicating that heart rate alone appears to be the main factor of determining the onset of TWA during submaximal exercise stress.