Effect of induced ventricular fibrillation and shock delivery on brain natriuretic peptide measured serially following a predischarge ICD test

Objectives

Brain natriuretic peptide (BNP) was a marker for heart failure and cardiac wall tension. We analysed the trend of BNP after predischarge testing in order to get non-invasive details about the cardiac stress during predischarge testing.

Methods

4-5 days after ICD implant we measured BNP, myoglobin, cardiac troponin I and creatine kinase in 20 patients before and 1, 5, 10, 20, 40, 60, 80, 100, 120 minutes and at the next day after predischarge testing. We evaluated actual values and percentage alterations of BNP.

Results

BNP significantly increased with a maximum after 5 minutes (804.0 ± 803.4 vs. 475.7 ± 629.5 pg/ml, P < 0.0001) and in terms of the percentage values (100 vs. 199.4 ± 61.4 %, P < 0.0001) compared with baseline BNP. BNP decreased after that with the last significantly increased BNP value after 20 minutes (540.2 ± 604.9 vs. 475.7 ± 629.5 pg/ml, P = 0.017). We excluded a cardiac necrosis during predischarge testing because of similar values of myoglobin, cardiac troponin I and creatine kinase during the 2-hour follow-up.

Conclusion

Our data showed a great increase with a doubling of BNP after 5 minutes as a result of induced ventricular fibrillation during predischarge test. This increase was not generated by myocardial necrosis but rather caused by an acute cardiac failure as a consequence of induced ventricular fibrillation in predischarge testing.     

Evaluation of Bachmann Bundle Pacing Versus Right Atrial Pacing in Prevention of Atrial Fibrillation After Coronary Artery Bypass Surgery

Background

In patients undergoing coronary artery bypass surgery (CABGS), occurrence of atrial fibrillation (AF) is common in the postoperative period and is associated with increased morbidity with longer intensive unit care (ICU) and hospital stay. Prevention with antiarrhythmic drugs is of limited success and associated with significant side effects. Therefore alternative approaches, such as Bachmann Bundle pacing, are required.

Methods and Results

154 consecutive patients, mean age 58±8.8 years, including 134 males and 20 females, were randomized to three groups; Group I : No pacing n= 54, Group II : RA pacing n= 52, Group III : Bachmann Bundle pacing n= 48. All the groups were well matched with regard to age, left atrial size, ejection fraction and use of beta blockers. Patients in Groups II and III were continually paced at a rate of 100 beats per minute (bpm) or at 10 bpm more than patients'' intrinsic heart rate. All the patients were monitored for 72 hours by telemetry and occurrence of AF was noted. Incidence of AF was 0% (none of 48 patients) in Group III as compared to 16.6% in Group I (9 of 54 patients) (p 0.003) and 12.5% in Group II (5 of 52 patients) (p 0.03). There was a trend towards shorter ICU stay in Group III (3.9 days) as compared to Group II (4.5 days) and Group I (4.1 days). Among the three groups, the reduction in mean P wave duration also was greater in Bachmann bundle paced group.

Conclusion

In patients undergoing CABGS, Bachmann bundle pacing is superior to right atrial / no pacing in the post operative period for preventing occurrence of AF and reducing ICU stay, commensurate with a reduction in mean P wave duration on surface ECG.     

A Low-Cost Simulation Model for R-Wave Synchronized Atrial Pacing in Pediatric Patients with Postoperative Junctional Ectopic Tachycardia

Background

Postoperative junctional ectopic tachycardia (JET) occurs frequently after pediatric cardiac surgery. R-wave synchronized atrial (AVT) pacing is used to re-establish atrioventricular synchrony. AVT pacing is complex, with technical pitfalls. We sought to establish and to test a low-cost simulation model suitable for training and analysis in AVT pacing.

Methods

A simulation model was developed based on a JET simulator, a simulation doll, a cardiac monitor, and a pacemaker. A computer program simulated electrocardiograms. Ten experienced pediatric cardiologists tested the model. Their performance was analyzed using a testing protocol with 10 working steps.

Results

Four testers found the simulation model realistic; 6 found it very realistic. Nine claimed that the trial had improved their skills. All testers considered the model useful in teaching AVT pacing. The simulation test identified 5 working steps in which major mistakes in performance test may impede safe and effective AVT pacing and thus permitted specific training. The components of the model (exclusive monitor and pacemaker) cost less than $50. Assembly and training-session expenses were trivial.

Conclusions

A realistic, low-cost simulation model of AVT pacing is described. The model is suitable for teaching and analyzing AVT pacing technique.     

Optimal Cardiac Resynchronization Therapy Pacing Rate in Non-Ischemic Heart Failure Patients: A Randomized Crossover Pilot Trial

Background

The optimal pacing rate during cardiac resynchronization therapy (CRT) is unknown. Therefore, we investigated the impact of changing basal pacing frequencies on autonomic nerve function, cardiopulmonary exercise capacity and self-perceived quality of life (QoL).

Methods

Twelve CRT patients with non-ischemic heart failure (NYHA class II–III) were enrolled in a randomized, double-blind, crossover trial, in which the basal pacing rate was set at DDD-60 and DDD-80 for 3 months (DDD-R for 2 patients). At baseline, 3 months and 6 months, we assessed sympathetic nerve activity by microneurography (MSNA), peak oxygen consumption (pVO₂), N-terminal pro-brain natriuretic peptide (p-NT-proBNP), echocardiography and QoL.

Results

DDD-80 pacing for 3 months increased the mean heart rate from 77.3 to 86.1 (p = 0.001) and reduced sympathetic activity compared to DDD-60 (51±14 bursts/100 cardiac cycles vs. 64±14 bursts/100 cardiac cycles, p<0.05). The mean pVO₂ increased non-significantly from 15.6±6 mL/min/kg during DDD-60 to 16.7±6 mL/min/kg during DDD-80, and p-NT-proBNP remained unchanged. The QoL score indicated that DDD-60 was better tolerated.

Conclusion

In CRT patients with non-ischemic heart failure, 3 months of DDD-80 pacing decreased sympathetic outflow (burst incidence only) compared to DDD-60 pacing. However, Qol scores were better during the lower pacing rate. Further and larger scale investigations are indicated.

Trial Registration

ClinicalTrials.gov NCT02258061     

Initial experience of a cohort of patients with hypertrophic cardiomyopathy undergoing biventricular pacing

Background

Dual chamber pacing improves functional status and reduces left ventricular outflow tract gradients in some, but not all patients with hypertrophic cardiomyopathy (HCM) by altering ventricular depolarisation. We investigated the use of biventricular (BIV) pacing in symptomatic patients with HCM.

Method

8 patients aged 58±7yrs with symptomatic HCM underwent BIV pacing. 5 patients had LVOT gradients >30mmHg. Ventricular electrodes were placed in the right ventricle (RV) and a branch of the coronary sinus. An atrial electrode was inserted to achieve BIV pacing with a short AV delay. The short-term effects of different pacing modalities were assessed using 2-D and Doppler echocardiography. Symptoms and exercise tolerance were assessed after a month of each pacing mode. Long-term follow up data was available for 5 years.

Results

Baseline EF was 67±14% and mean QRS duration was 132±26msecs. BIV pacing reduced QRS duration compared to RV pacing (129±46 vs. 205±54msecs, p<0.005). Five of the seven patients had baseline LVOT gradients (mean 67±25mmHg) that decreased to 41±15mm Hg with RV pacing (p<0.01) and 25±15mmHg with BIV pacing (p<0.005). Improvements in exercise time with active pacing occurred in six out of eight patients (75%), three (37.5%) had optimal exercise times with RV pacing and three with BIV pacing. Of the three patients with short term improvements with BIV pacing, one died 4 years post implant, one deteriorated with LV dilatation and one had the system explanted for infection.

Conclusion

BIV pacing showed short-term beneficial effects in some patients over and above RV pacing alone.     

Pacemaker Dependency after Cardiac Surgery: A Systematic Review of Current Evidence

Background

Severe postoperative conduction disturbances requiring permanent pacemaker implantation frequently occur following cardiac surgery. Little is known about the long-term pacing requirements and risk factors for pacemaker dependency in this population.

Methods

We performed a systematic review of the literature addressing rates and predictors of pacemaker dependency in patients requiring permanent pacemaker implantation after cardiac surgery. Using a comprehensive search of the Medline, Web of Science and EMBASE databases, studies were selected for review based on predetermined inclusion and exclusion criteria.

Results

A total of 8 studies addressing the endpoint of pacemaker-dependency were identified, while 3 studies were found that addressed the recovery of atrioventricular (AV) conduction endpoint. There were 10 unique studies with a total of 780 patients. Mean follow-up ranged from 6–72 months. Pacemaker dependency rates ranged from 32%-91% and recovery of AV conduction ranged from 16%-42%. There was significant heterogeneity with respect to the definition of pacemaker dependency. Several patient and procedure-specific variables were found to be independently associated with pacemaker dependency, but these were not consistent between studies.

Conclusions

Pacemaker dependency following cardiac surgery occurs with variable frequency. While individual studies have identified various perioperative risk factors for pacemaker dependency and non-resolution of AV conduction disease, results have been inconsistent. Well-conducted studies using a uniform definition of pacemaker dependency might identify patients who will benefit most from early permanent pacemaker implantation after cardiac surgery.     

Heart Rate Variability Analysis in an Experimental Model of Hemorrhagic Shock and Resuscitation in Pigs

Background

The analysis of heart rate variability (HRV) has been shown as a promising non-invasive technique for assessing the cardiac autonomic modulation in trauma. The aim of this study was to evaluate HRV during hemorrhagic shock and fluid resuscitation, comparing to traditional hemodynamic and metabolic parameters.

Methods

Twenty anesthetized and mechanically ventilated pigs were submitted to hemorrhagic shock (60% of estimated blood volume) and evaluated for 60 minutes without fluid replacement. Surviving animals were treated with Ringer solution and evaluated for an additional period of 180 minutes. HRV metrics (time and frequency domain) as well as hemodynamic and metabolic parameters were evaluated in survivors and non-survivors animals.

Results

Seven of the 20 animals died during hemorrhage and initial fluid resuscitation. All animals presented an increase in time-domain HRV measures during haemorrhage and fluid resuscitation restored baseline values. Although not significantly, normalized low-frequency and LF/HF ratio decreased during early stages of haemorrhage, recovering baseline values later during hemorrhagic shock, and increased after fluid resuscitation. Non-surviving animals presented significantly lower mean arterial pressure (43±7vs57±9 mmHg, P<0.05) and cardiac index (1.7±0.2vs2.6±0.5 L/min/m², P<0.05), and higher levels of plasma lactate (7.2±2.4vs3.7±1.4 mmol/L, P<0.05), base excess (-6.8±3.3vs-2.3±2.8 mmol/L, P<0.05) and potassium (5.3±0.6vs4.2±0.3 mmol/L, P<0.05) at 30 minutes after hemorrhagic shock compared with surviving animals.

Conclusions

The HRV increased early during hemorrhage but none of the evaluated HRV metrics was able to discriminate survivors from non-survivors during hemorrhagic shock. Moreover, metabolic and hemodynamic variables were more reliable to reflect hemorrhagic shock severity than HRV metrics.     

Left Atrial Size and Function in a Canine Model of Chronic Atrial Fibrillation and Heart Failure

Background

Our aim was to assess how atrial fibrillation (AF) induction, chronicity, and RR interval irregularity affect left atrial (LA) function and size in the setting of underlying heart failure (HF), and to determine whether AF effects can be mitigated by vagal nerve stimulation (VNS).

Methods

HF was induced by 4-weeks of rapid ventricular pacing in 24 dogs. Subsequently, AF was induced and maintained by atrial pacing at 600 bpm. Dogs were randomized into control (n = 9) and VNS (n = 15) groups. In the VNS group, atrioventricular node fat pad stimulation (310 μs, 20 Hz, 3–7 mA) was delivered continuously for 6 months. LA volume and LA strain data were calculated from bi-weekly echocardiograms.

Results

RR intervals decreased with HF in both groups (p = 0.001), and decreased further during AF in control group (p = 0.014), with a non-significant increase in the VNS group during AF. LA size increased with HF (p<0.0001), with no additional increase during AF. LA strain decreased with HF (p = 0.025) and further decreased after induction of AF (p = 0.0001). LA strain decreased less (p = 0.001) in the VNS than in the control group. Beat-by-beat analysis showed a curvilinear increase of LA strain with longer preceding RR interval, (r = 0.45, p <0.0001) with LA strain 1.1% higher (p = 0.02) in the VNS-treated animals, independent of preceding RR interval duration. The curvilinear relationship between ratio of preceding and pre-preceding RR intervals, and subsequent LA strain was weaker, (r = 0.28, p = 0.001). However, VNS-treated animals again had higher LA strain (by 2.2%, p = 0.002) independently of the ratio of preceding and pre-preceding RR intervals.

Conclusions

In the underlying presence of pacing-induced HF, AF decreased LA strain, with little impact on LA size. LA strain depends on the preceding RR interval duration.     

Relationship between Inflammatory Cytokines and Indices of Cardiac Dysfunction following Intense Endurance Exercise

Objectives

Pro-inflammatory cytokines have been noted to increase following exercise but their relationship to exercise-induced cardiac dysfunction has not previously been investigated. We sought to evaluate whether exercise-induced cardiac dysfunction was associated with increases in cytokines, particularly the pro-inflammatory cytokines IL-1β, IL-12p70 and TNFα, which have been most implicated in cardiac pathology.

Methods

40 well-trained endurance athletes underwent evaluation prior to and immediately following one of four endurance sporting events ranging from 3 to 11 hours duration. Cytokines (IL-1β, IL-6, IL-8, IL-10, IL-12p70 and TNFα) were analyzed by flow cytometry from serum samples collected within 50 minutes of race completion. Cardiac troponin (cTnI) and B-type natriuretic peptide were combined with an echocardiographic assessment of cardiac function, and a composite of cTnI > 0.04 μg/L, BNP increase > 10 ng/L and a decrease in right ventricular ejection (RVEF) > 10% were prospectively defined as evidence of myocardial dysfunction.

Results

Relative to baseline, IL-6 IL-8 and IL-10 increased 8.5-, 2.9-, and 7.1-fold, respectively, P<0.0001. Thirty-one (78%), 19 (48%) and 18 (45%) of the athletes met the pre-specified criteria for significant cTnI, BNP and RVEF changes, respectively. TNFα, IL-12p70 were univariate predictors of ΔRVEF and ΔBNP whilst none of the anti-inflammatory cytokines were significantly associated with these measures. Ten athletes (25%, all athletes competing in the endurance event of longest duration) met criteria for exercise-induced myocardial dysfunction. In these 10 athletes with myocardial dysfunction, as compared to those without, there was significantly greater post-race expression of the pro-inflammatory cytokines IL-12p70 (8.1±3.8pg/ml vs. 2.5±2.6pg/ml, P<0.0001) and TNFα (6.5±3.1pg/ml vs. 2.0±2.5pg/ml, P<0.0001).

Conclusion

Cardiac dysfunction following intense endurance exercise was associated with increased expression of pro-inflammatory cytokines. This does not prove a causal relationship but provides rationale for further investigations into whether inflammation mediates exercise-induced myocardial dysfunction.     

The Effects Of Short Time Right Ventricular Pacing On Left Atrial Mechanical Functions

Objectives

Left atrium (LA) plays an important role in left ventricular filling. It is well known that right ventricular apical pacing has unfavorable effects on ventricular systolic and diastolic performance. The aim of this study is to evaluate the LA mechanical functions with 2D echocardiography in patients with a permanent pacemaker after short time ventricular pacing.

Design

Echocardiographic examination was performed in 38 patients (mean age 63.0± 10.9, 18 female) with dual chamber pacemakers or defibrillators (< 20% ventricular pacing within previous 6 months, all of them on sinus rhythm) before and after 4 hours > 90% ventricular pacing at 70 beats per minute in DDD mode with an optimal AV interval. Left atrial volumes (LAV) including at the time of mitral valve opening (Vmax), at closure (Vmin), and at the onset of atrial systole (Volp) were measured. The passive emptying, conduit, active emptying and total emptying volume, stroke volumes were also calculated.

Results

No significant differences were noted at baseline and after pacing for absolute Vmax, Volp, passive emptying, conduit, active emptying, total emptying volumes as well as the volumes indexed to body surface area (p >0.05).

Conclusions

Short - time RV pacing seems to have no acute effects on left atrial mechanical functions.     

Anodal stimulation: an underrecognized cause of nonresponders to cardiac resynchronization therapy

Objective

The purpose of this study was to determine if anodal stimulation accounts for failure to benefit from cardiac resynchronization therapy (CRT) in some patients.

Background

Approximately 30-40% of patients with moderate to severe heart failure do not have symptomatic nor echocardiographic improvement in cardiac function following CRT. Modern CRT devices allow the option of programming left ventricular (LV) lead pacing as LV tip to right ventricular (RV) lead coil to potentially improve pacing thresholds. However, anodal stimulation can result in unintentional RV pacing (anode) instead of LV pacing (cathode).

Methods

Patients enrolled in our center''s CRT registry had an echocardiogram, 6-minute walk (6MW), and Minnesota Living with HF Questionnaire (MLHFQ) pre-implant and 6 months after CRT. Electrocardiograms (12 lead) during RV, LV, and biventricular (BiV) pacing were obtained at the end of the implant in 102 patients. Anodal stimulation was defined as LV pacing QRS morphology on EKG being identical to RV pacing or consistent with fusion with RV and LV electrode capture. LV end systolic volume (LVESV) was measured by echo biplane Simpson''s method and CRT responder was defined as 15% or greater reduction in LVESV.

Results

Of the 102 patients, 46 (45.1%) had the final LV lead pacing configuration programmed LV (tip or ring) to RV (coil or ring). 3 of the 46 subjects (6.5%) had EKG findings consistent with anodal stimulation, not corrected intraoperatively. All anodal stimulation patients were nonresponders to CRT by echo criteria (reduction in LVESV 13.3 ± 0.6%, increase in EF 5.0 ± 1.4%) compared to 46% responders for those without anodal stimulation, (change in LVESV 18.7 ± 25.6%, EF 7.6 ±10.9%). None of the anodal stimulation patients were responders for the 6 minute walk, compared to 32 of 66 (48%) of those without anodal stimulation.

Conclusion

Anodal stimulation is a potential underrecognized and ameliorable cause of poor response to CRT.     

Haemodynamic evaluation of alternative left ventricular endocardial pacing sites in clinical non-responders to cardiac resynchronisation therapy

Introduction

Non response to cardiac resynchronisation therapy (CRT) may be related to the position of the coronary sinus lead.

Methods

We studied the acute haemodynamic response (AHR) from alternative left ventricular (LV) endocardial pacing sites in clinical non-responders to CRT. AHR and the interval from QRS onset to LV sensing (Q-LV interval) from four different endocardial pacing sites were evaluated in 24 clinical non-responders. A rise in LVdP/dtmax ≥ 15 % from baseline was considered a positive AHR. We also compared the AHR from endocardial with the corresponding epicardial lead position.

Results

The implanted system showed an AHR ≥ 15 % in 5 patients. In 9 of the 19 remaining patients, AHR could be elevated to ≥ 15 % by endocardial LV pacing. The optimal endocardial pacing site was posterolateral. There was no significant difference in AHR between the epicardial and the corresponding endocardial position. The longest Q-LV interval corresponded with the best AHR in 12 out of the 14 patients with a positive AHR, with an average Q-LV/QRS width ratio of 90 %.

Conclusions

Acute haemodynamic testing may indicate an alternative endocardial pacing site with a positive AHR in clinical non-responders. The Q-LV interval is a strongly correlated with the optimal endocardial pacing site. Endocardial pacing opposite epicardial sites does not result in a better AHR.     

Neutral endopeptidase inhibitor suppresses the early phase of atrial electrical remodeling in a canine rapid atrial pacing model

Introduction

We examined the acute effects of neutral endopeptidase inhibitor on the hemodynamics and electrical properties of dogs subjected to rapid atrial pacing.

Methods

Ten beagle dogs were used and divided into two groups with and without candoxatril, a neutral endopeptidase inhibitor preadministration. Before and after the 6 hours rapid atrial pacing from the right atrial appendage, the hemodynamics, atrial effective refractory period, and monophasic action potential duration of the right atrial appendage were measured and blood samples were collected. Atrial tissue was also excised after the experiment.

Results

Candoxatril significantly increased plasma ANP levels (Control: 88.4 ± 50.25 vs. Candoxatril: 197.1 ± 32.09 pg/ml, p = 0.004) and prevented reductions in atrial effective refractory period and monophasic action potential duration. We further demonstrated that the treated animals exhibited significantly higher levels of atrial tissue cyclic GMP (Control: 28.1 ± 1.60 fmol/mg vs. Candoxatril: 44.5 ± 12.28 fmol/mg, p = 0.034) as well as that of plasma cyclic GMP (Control: 32 ± 5.5 vs. Candoxatril: 42 ± 7.1 pg/ml, p = 0.028).

Conclusion

Candoxatril suppressed the shortening of atrial effective refractory period and monophasic action potential duration in the rapid atrial pacing model. As plasma ANP and the atrial tissue levels of cyclic GMP were higher in the Candoxatril group than the control, this effect was considered to appear through the reduction of calcium overload caused by ANP and cyclic GMP.     

Shortening of atrioventricular delay at increased atrial paced heart rates improves diastolic filling and functional class in patients with biventricular pacing

Background

Use of rate adaptive atrioventricular (AV) delay remains controversial in patients with biventricular (Biv) pacing. We hypothesized that a shortened AV delay would provide optimal diastolic filling by allowing separation of early and late diastolic filling at increased heart rate (HR) in these patients.

Methods

34 patients (75 ± 11 yrs, 24 M, LVEF 34 ± 12%) with Biv and atrial pacing had optimal AV delay determined at baseline HR by Doppler echocardiography. Atrial pacing rate was then increased in 10 bpm increments to a maximum of 90 bpm. At each atrial pacing HR, optimal AV delay was determined by changing AV delay until best E and A wave separation was seen on mitral inflow pulsed wave (PW) Doppler (defined as increased atrial duration from baseline or prior pacemaker setting with minimal atrial truncation). Left ventricular (LV) systolic ejection time and velocity time integral (VTI) at fixed and optimal AV delay was also tested in 13 patients. Rate adaptive AV delay was then programmed according to the optimal AV delay at the highest HR tested and patients were followed for 1 month to assess change in NYHA class and Quality of Life Score as assessed by Minnesota Living with Heart Failure Questionnaire.

Results

81 AV delays were evaluated at different atrial pacing rates. Optimal AV delay decreased as atrial paced HR increased (201 ms at 60 bpm, 187 ms at 70 bpm, 146 ms at 80 bpm and 123 ms at 90 bpm (ANOVA F-statistic = 15, p = 0.0010). Diastolic filling time (P < 0.001 vs. fixed AV delay), mitral inflow VTI (p < 0.05 vs fixed AV delay) and systolic ejection time (p < 0.02 vs. fixed AV delay) improved by 14%, 5% and 4% respectively at optimal versus fixed AV delay at the same HR. NYHA improved from 2.6 ± 0.7 at baseline to 1.7 ± 0.8 (p < 0.01) 1 month post optimization. Physical component of Quality of Life Score improved from 32 ± 17 at baseline to 25 ± 12 (p < 0.05) at follow up.

Conclusions

Increased heart rate by atrial pacing in patients with Biv pacing causes compromise in diastolic filling time which can be improved by AV delay shortening. Aggressive AV delay shortening was required at heart rates in physiologic range to achieve optimal diastolic filling and was associated with an increase in LV ejection time during optimization. Functional class improved at 1 month post optimization using aggressive AV delay shortening algorithm derived from echo-guidance at the time of Biv pacemaker optimization.     

Measurement of Myocardial T1ρ with a Motion Corrected,Parametric Mapping Sequence in Humans

Purpose

To develop a robust T_1ρ magnetic resonance imaging (MRI) sequence for assessment of myocardial disease in humans.

Materials and Methods

We developed a breath-held T_1ρ mapping method using a single-shot, T_1ρ-prepared balanced steady-state free-precession (bSSFP) sequence. The magnetization trajectory was simulated to identify sources of T_1ρ error. To limit motion artifacts, an optical flow-based image registration method was used to align T_1ρ images. The reproducibility and accuracy of these methods was assessed in phantoms and 10 healthy subjects. Results are shown in 1 patient with pre-ventricular contractions (PVCs), 1 patient with chronic myocardial infarction (MI) and 2 patients with hypertrophic cardiomyopathy (HCM).

Results

In phantoms, the mean bias was 1.0 ± 2.7 msec (100 msec phantom) and 0.9 ± 0.9 msec (60 msec phantom) at 60 bpm and 2.2 ± 3.2 msec (100 msec) and 1.4 ± 0.9 msec (60 msec) at 80 bpm. The coefficient of variation (COV) was 2.2 (100 msec) and 1.3 (60 msec) at 60 bpm and 2.6 (100 msec) and 1.4 (60 msec) at 80 bpm. Motion correction improved the alignment of T_1ρ images in subjects, as determined by the increase in Dice Score Coefficient (DSC) from 0.76 to 0.88. T_1ρ reproducibility was high (COV < 0.05, intra-class correlation coefficient (ICC) = 0.85–0.97). Mean myocardial T_1ρ value in healthy subjects was 63.5 ± 4.6 msec. There was good correspondence between late-gadolinium enhanced (LGE) MRI and increased T_1ρ relaxation times in patients.

Conclusion

Single-shot, motion corrected, spin echo, spin lock MRI permits 2D T_1ρ mapping in a breath-hold with good accuracy and precision.     

Plasma Free Hemoglobin Is an Independent Predictor of Mortality among Patients on Extracorporeal Membrane Oxygenation Support

Background

Hemolysis is common in all extracorporeal circuits as evident by the elevated plasma free hemoglobin (PFHb) level. We investigated whether increased hemolysis during extracorporeal membrane oxygenation (ECMO) is an independent mortality predictor.

Methods

We performed a retrospective observational study of consecutive subjects who received ECMO at a tertiary care facility from 2007-2013 to investigate independent predictors of in-hospital mortality. We examined variables related to patient demographics, comorbidities, markers of hemolysis, ECMO characteristics, transfusion requirements, and complications. 24-hour PFHb> 50 mg/dL was used as a marker of severe hemolysis.

Results

154 patients received ECMO for cardiac (n= 115) or pulmonary (n=39) indications. Patients’ mean age was 51 years and 75.3% were males. Compared to nonsurvivors, survivors had lower pre-ECMO lactic acid (p=0.026), lower 24-hour lactic acid (p=0.023), shorter ECMO duration (P=0.01), fewer RBC transfusions on ECMO (p=0.008) and lower level of PFHb 24-hours post ECMO implantation (p=0.029). 24-hour PFHb> 50 mg/dL occurred in 3.9 % versus 15.5% of survivors and nonsurvivors, respectively, p=0.002. A Cox proportional hazard analysis identified PFHb> 50 mg/dL 24-hours post ECMO as an independent predictor of mortality (OR= 3.4, 95% confidence interval: 1.3 – 8.8, p= 0.011).

Conclusion

PFHb> 50 mg/dL checked 24-hour post ECMO implantation is a useful tool to predict mortality. We propose the routine checking of PFHb 24-hours after ECMO initiation for early identification and treatment of the cause of hemolysis.     

Impact of Heart Rate on Myocardial Salvage in Timely Reperfused Patients with ST-Segment Elevation Myocardial Infarction: New Insights from Cardiovascular Magnetic Resonance

Background

Previous studies evaluating the progression of the necrotic wave in relation to heart rate were carried out only in animal models of ST-elevated myocardial infarction (STEMI). Aim of the study was to investigate changes of myocardial salvage in relation to different heart rates at hospital admission in timely reperfused patients with STEMI by using cardiovascular magnetic resonance (CMR).

Methods

One hundred-eighty-seven patients with STEMI successfully and timely treated with primary coronary angioplasty underwent CMR five days after hospital admission. According to the heart rate at presentation, patients were subcategorized into 5 quintiles: <55 bpm (group I, n = 44), 55–64 bpm (group II, n = 35), 65–74 bpm (group III, n = 35), 75–84 bpm (group IV, n = 37), ≥85 bpm (group V, n = 36). Area at risk, infarct size, microvascular obstruction (MVO) and myocardium salvaged index (MSI) were assessed by CMR using standard sequences.

Results

Lower heart rates at presentation were associated with a bigger amount of myocardial salvage after reperfusion. MSI progressively decreased as the heart rates increased (0.54 group I, 0.46 group II, 0.38 group III, 0.34 group IV, 0.32 group V, p<0.001). Stepwise multivariable analysis showed heart rate, peak troponin and the presence of MVO were independent predictor of myocardial salvage. No changes related to heart rate were observed in relation to area at risk and infarct size.

Conclusions

High heart rates registered before performing coronary angioplasty in timely reperfused patients with STEMI are associated with a reduction in salvaged myocardium. In particular, salvaged myocardium significantly reduced when heart rate at presentation is ≥85 bpm.     

Isthmus Dependent Atrial Flutter Cycle Length Correlates with Right Atrial Cross-Sectional Area

Background

Right atrial flutter cycle length can prolong in the presence of antiarrhythmic drug therapy. We hypothesized that the cycle length of right atrial isthmus dependent flutter would correlate with right atrial cross-sectional area measurements.

Methods

60 patients who underwent ablation for electrophysiologically proven isthmus dependent right atrial flutter, who were not on Class I or Class III antiarrhythmic drugs and had recent 2-dimensional echocardiographic data comprised the study group. Right atrial length and width were measured in the apical four chamber view. Cross-sectional area was estimated by multiplying the length and width. 35 patients had an atrial flutter rate ≥ 250 bpm (Normal Flutter Group) and 25 patients had an atrial flutter rate < 250 bpm (Slow Flutter Group).

Results

Mean atrial flutter rate was 283 bpm in the normal flutter group and 227 bpm in the slow flutter group. Mean atrial flutter cycle length was 213 ms in the Normal Flutter Group and 265 ms in the Slow Flutter Group (p< 0.0001). Mean right atrial cross sectional area was 1845 mm² in the Normal Flutter group and 2378 mm² in the Slow Flutter Group, (p< 0.0001). Using linear regression, CSA was a significant predictor of cycle length (β =0.014 p = 0.0045). For every 1 mm² increase in cross-sectional area, cycle length is 0.014 ms longer.

Conclusions

In the absence of antiarrhythmic medications, right atrial cross sectional area enlargement correlates with atrial flutter cycle length. These findings provide further evidence that historical rate-related definitions of typical isthmus dependent right atrial are not mechanistically valid.     

Assessment of Brainstem Function with Auricular Branch of Vagus Nerve Stimulation in Parkinson’s Disease

Background

The efferent dorsal motor nucleus of the vagal nuclei complex may degenerate early in the course of Parkinson’s disease (PD), while efferent nucleus ambiguous, the principal source of parasympathetic vagal neurons innervating the heart, and afferent somatosensory nuclei remain intact.

Objective

To obtain neurophysiological evidence related to this pattern, we tested processing of afferent sensory information transmitted via the auricular branch of the vagus nerve (ABVN) which is known to be connected to autonomic regulation of cardiac rhythm.

Methods

In this cross-sectional observational study, we recorded (i) somatosensory evoked potentials (ABVN-SEP) and (ii) cutaneo-cardioautonomic response elicited by stimulation of the ABVN (modulation of heart-rate variability (HRV index; low frequency power, ln(LF), high frequency power, ln(HF); ln(LF/HF) ratio)) in 50 PD patients and 50 age and sex matched healthy controls. Additionally, auditory evoked potentials and trigeminal nerve SEP were assessed.

Results

Neither ABVN-SEP nor any of the other functional brainstem parameters differed between patients and controls. Although HRV index was decreased in PD patients, modulation of ln(LF/HF) by ABVN-stimulation, likely indicating cardiac parasympathetic activation, did not differ between both groups.

Conclusions

Findings do not point to prominent dysfunction of processing afferent information from ABVN and its connected parasympathetic cardiac pathway in PD. They are consistent with the known pattern of degeneration of the vagal nuclei complex of the brainstem.