Hannu Parikka

Arrhythmias and heart rate variability during and after therapeutic hypothermia for cardiac arrest.

Objective:To evaluate the effects of therapeutic hypothermia (HT) of 33°C after cardiac arrest (CA) on cardiac arrhythmias, heart rate variability (HRV), and their prognostic value. Design:Prospective, comparative substudy of a randomized controlled trial of mild HT after out-of-hospital CA, the European Hypothermia After Cardiac Arrest study. Setting:Intensive care unit of a tertiary referral hospital (Helsinki University Hospital). Patients:Seventy consecutive adult patients resuscitated from out-of-hospital ventricular fibrillation were randomly assigned either to therapeutic HT of 33°C or normothermia. Interventions:Patients randomized to HT were cooled with an external cooling device for 24 hours and then allowed to rewarm slowly during 12 hours. In the normothermia group, the core temperature was kept <38°C by antipyretics and physical means. All patients received standard intensive care for at least 2 days. Measurements and Main Results:Twenty-four hour ambulatory electrocardiography recordings were performed at 0–24 hours, at 24–48 hours, and at 14 days. The clinical outcome was assessed at 6 months after CA. The occurrence of premature ventricular beats was increased in the HT-treated group during the first two recordings, with no difference in the number of ventricular tachycardia or ventricular fibrillation episodes. All HRV values were significantly higher during the HT (p < 0.01), but no differences were observed 2 weeks later. In multivariate analysis, only shorter delay to restoration of spontaneous circulation (p = 0.009) and the sd of individual normal-to-normal intervals >100 msec of the 24–48-hour recording in the HT group (p = 0.018) predicted good outcome. Conclusions:The use of therapeutic HT of 33°C for 24 hours after CA was not associated with an increase in clinically significant arrhythmias. Preserved 24 to 48-hour HRV may be a predictor of favorable outcome in patients with CA treated with HT.

Transcardiac gradients of N-terminal B-type natriuretic peptide in aortic valve stenosis.

Plasma B‐type natriuretic peptide (BNP), as well as the N‐terminal part of the prohormone (Nt‐BNP), are frequently elevated in aortic valve stenosis (AS). Yet, their release from the heart into the circulation has never been directly studied in AS.

Non-invasive detection of conduction pathways to left atrium using magnetocardiography: validation by intra-cardiac electroanatomic mapping

AIMS Alteration in conduction from right to left atrium (LA) is linked to susceptibility to atrial fibrillation (AF). We examined whether different inter-atrial conduction pathways can be identified non-invasively by magnetocardiographic mapping (MCG). METHODS AND RESULTS In 27 patients undergoing catheter ablation of paroxysmal AF, LA activation sequence was determined during sinus rhythm using invasive electroanatomic mapping. Before this, 99-channel magnetocardiography was recorded over anterior chest. The orientation of the magnetic fields during the early (40-70 ms from P onset) and later part (last 50%) of LA depolarization was determined using pseudocurrent conversion. Breakthrough of electrical activation to LA occurred through Bachmann bundle (BB) in 14, margin of fossa ovalis (FO) in 3, coronary sinus ostial region (CS) in 2, and their combinations in 10 cases by invasive reference in total of 29 different P-waves. Based on the combination of pseudocurrent angles over early and late parts of LA activation, the MCG maps were divided to three types. These types correctly identified the LA breakthrough sites to BB, CS, FO, or their combinations in 27 of 29 (93%) cases. CONCLUSION Magnetocardiographic mapping seems capable of distinguishing inter-atrial conduction pathways. Recognizing the inter-atrial conduction pattern may assist in understanding the pathogenesis of AF and identifying the subgroups for patient-tailored therapy.

Reversal of Atrial Remodeling after Cardioversion of Persistent Atrial Fibrillation Measured with Magnetocardiography

Background: Atrial fibrillation (AF) causes electrical, functional, and structural changes in the atria. We examined electrophysiologic remodeling caused by AF and its reversal noninvasively by applying a new atrial signal analysis based on magnetocardiography (MCG).

Ventricular Arrhythmia Suppression by Magnesium Treatment after Coronary Artery Bypass Surgery.

Ventricular arrhythmias occur frequently shortly after coronary artery bypass grafting (CABG), and their occurrence coincides with the postoperative decline in serum magnesium (Mg) levels. To examine if this decline causes ventricular arrhythmias and if their appearance could be reduced by intravenous Mg administration, 140 consecutive CABG patients were randomized to receive 70 mmol of Mg sulphate (N=69) or placebo (N=71) over two days. Serum Mg concentration fell to 0.77 mmol/l in the control group but rose to 1.09 mmol/l in the Mg group (p<0.001). On 48 h Holter, the number of ventricular premature complexes (VPC) on the third postoperative day was reduced in the Mg group (4±5 vs 12±21 VPCs/h;p<0.05) and the incidence of complex ventricular arrhythmias (Lown grade 2–5) was significantly diminished (19% vs 41% of the patients;p<0.05). In multivariate analysis, high risk ventricular arrhythmias (repetitive polymorphic ventricular complexes, couplets, R-on-T complexes or operative tachycardia) were independently predicted by high number of bypassed vessels (p=0.01), poor NYHA functional class (p=0.06), preoperative diuretic use (p=0.07), and low postoperative Mg levels (p=0.08). In conclusion, correction of the postoperative decline in serum Mg concentration decreases the occurrence of early VPCs and complex ventricular arrhythmias. Patients with extensive underlying coronary artery disease and prior diuretic therapy appear to benefit greatest from Mg treatment.

Atrial refractoriness and action potential duration after sudden reversal of atrioventricular sequence

To address the potential of atrioventricular (AV) asynchrony to provoke cardiac arrhythmias, atrial electrophysiology was examined during normal and reversed AV interval in anesthetized pigs. A new automatic stimulation technique was adapted to monitor rapid changes in the effective refractory period (ERP), using continuous AV sequential pacing, incremental extrastimulus interval scanning, and automatic detection of capture. Right atrial ERP using 2–8 ms stimulus interval increments and right atrial and ventricular monophasic action potential (MAP) duration were determined simultaneously when the AV interval was changed from normal (+80 ms) to reversed (−40 ms) and back. During reversed AV interval the peak right atrial pressure increased from 8 ± 3 to 14 ± 4 mmHg (P < 0.001) and mean arterial pressure decreased from 86 ± 18 to 65 ± 21 mmHg (P < 0.001). At new steady state, atrial ERP and MAP duration at 90% level of repolarization were lengthened by 22 ± 16 and 42 ± 12 ms respectively (P < 0.001). Ventricular MAP duration did not change. A statistically significant lengthening in atrial ERP could be demonstrated in 5–10 seconds. After reversion of the AV sequence, the ratio of atrial ERP to MAP duration decreased from 1.27 to 0.94 (P < 0.001) on average for 15 seconds, the change being thought to favor reentry. Thus atrial wall stress from contraction during ventricular systole even for a short period of time modifies atrial electrophysiology. Deficient AV synchrony may immediately contribute to the development of atrial arrhythmias. (PACE 2004; 27:10–18)

Detection of Rapid Changes in Ventricular Refractoriness in Human Studies

TOIVONEN, L., et al.: Detection of Rapid Changes in Ventricular Refractoriness in Human Studies. Conventional determination of the ventricular effective refractory period (VERP) is unsuitable for detection of rapid fluctuations in the effective refractory period (ERP). A programmed stimulation system was developed that adapts continuous atrioventricular sequential pacing, incremental extrastimulus interval (S1S2) scanning, and automatic detection of extrastimulus capture which is followed by shortening of S1S2 to execute repeated scanning. The accuracy of ERP determination was tested using variable incremental (2 and 4 ms) and decremental (4–16 ms) steps of the S1S2 interval. Based on a mean of 82 determinations in eight patients, the average VERP values stayed at 249.8–251.0 ms except during the highest capture frequency. Standard deviation of ERP values ranged from 1.1 to 2.5 ms on average at the tested incremental and decremental steps. One determination was accomplished within 7.8–15.6 seconds on average. The ability to track changes in ERP was tested by changing the drive cycle length. Time constants for the adaptation rate of VERP and ventricular monophasic action potential duration at a 90% level of repolarization were determined from each test, and were similar, 51 ± 8 seconds (mean ± SEM) for ERP and 51 ± 6 seconds for the action potential duration. Thus, the developed method provides accurate ERP measurements during rapid variation in ventricular refractoriness. It allows studying the recovery of excitability and the action potential duration simultaneously, and would be valuable particularly in pathological conditions and pharmacologic interventions where these electrophysiological variables become dissociated.

Acute effects of intravenous magnesium on ventricular refractoriness and monophasic action potential duration in humans.

The objective of this study was to examine the antiarrhythmic mechanisms of magnesium (Mg). The 12 patients who were selected for the study were given 12 mmol Mg sulphate followed by an infusion of 8 mmol/h. Ventricular effective refractory period (VERP). monophasic action potential duration at 50% and 90% repolarization during spontaneous rhythm (MAPD50, MAPD90) and atrial pacing at a cycle length of 600 ms (MAPD(50)600, MAPD(90)600) were measured before and after the intervention. Plasma magnesium concentration rose from 0.83 +/- 0.05 to 1.85 +/- 0.24 mmol/l (p < 0.001). Shortening of MAPD(50) (250 +/- 45 vs 240 +/- 46 ms; p < 0.05), MAPD(90) (294 +/- 42 vs 283 +/- 41 ms; p < 0.05) and shortening of sinus cycle length (SCL) (783 +/- 153 vs 742 +/- 160 ms; p < 0.01) were detected. During controlled cycle length, magnesium decreased MAPD(50)600 (230 +/- 28 vs 221 +/- 28 ms; p < 0.01), MAPD(90)600 (274 +/- 25 vs 261 +/- 29 ms; p < 0.01) and VERP (247 +/- 25 vs 241 +/- 21 ms: p < 0.05). QRS duration, QT interval and blood pressure remained unchanged. The change in SCL correlated with the change in MAPD(50) (r = 0.58; p < 0.05) and MAPD(90) (r = 0.55; p = 0.06 ) but not with MAPD(50)600, MAPD(90)600 or VERP. Magnesium acutely shortens ventricular monophasic action potential duration and refractoriness. This effect is partly mediated by mechanisms that increase heart rate. The reductions might bring salutary effects in arrhythmias evoked by prolonged repolarization.

Noninvasive mapping reveals recurrent and suddenly changing patterns in atrial fibrillation—a magnetocardiographic study

OBJECTIVE To study noninvasive magnetocardiographic (MCG) mapping of ongoing atrial fibrillation (AF) and, for the possible mapping patterns observed, to develop simplified but meaningful descriptors or parameters, providing a possible basis for future research and clinical use of the mappings. APPROACH MCG mapping with simultaneous ECG was recorded during arrhythmia in patients representing a range of typical, clinically classical atrial arrhythmias. The recordings were assessed using MCG map animations, and a method to compute magnetic field map orientation (MFO) and its time course was created to facilitate presentation of the findings. All the data were segmented into four categories of ECG waveform regularity. MAIN RESULTS In visual observation of the MCG animations, an abundance of clear spatial and temporal patterns with regularity were found, often perceived as rotations of the map. This rotation and its sudden reversals of direction were distinctly present in the time course of the MFO. The shortest segments with consistent rotation lasted for some hundreds of milliseconds, i.e. a couple of cycles, but segments lasting for tens of seconds were observed as well. In the ECG, all four categories of regularity were present. The rotation of the MFO was observed in all patients under study and regardless of the ECG categories. Further, a change in ECG category during a measurement was frequently, but not always, found to be simultaneous with a change in the rotation pattern of the MFO. Utilization of spatial information of MCG mapping could enable detection of both regularities and instantaneous phenomena during AF. SIGNIFICANCE Cardiac mapping may offer a useful noninvasive means to study the mechanisms of AF, including superior temporal resolution.